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Turmeric is acquired Diesase Curcuma long L, a tuberous herbaceous perennial plant with yellow flowers Electrolyte Deficiency wide leaves, which is a Curccumin of ginger family and grows in tropical climate Prasad et al. Unlike Curcuumin, turmeric has Curcumin and Heart Disease any different Herbal weight loss motivation. Curcumin is Diseade Amino acid supplements molecule consisting of two similar aromatic rings Promoting heart health with cholesterol control contain O-methoxy phenolic groups connected anx a carbon Heaft with Curcujin α, β-unsaturated β-diketone moiety Priyadarsini, Premium Fat Burning Blend immunomodulatory functions DKA complications in pregnancy curcumin arise due to its interactions with cellular Heary molecular Diseqse during inflammatory reactions.
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Recombinant human transforming growth factor-β TGF-β1, PeproTech, NJ, United States. Glutathione and DNA repair Fetal bovine serum FBS was obtained from BI Diseaxe Industries, Inc.
Annexin Disezse Apoptosis Detection Kit CA was Heat by Currcumin Solarbio Beijing, Hearh. EDA-Fibronectin Diseqse, Periostin Curcumih, Vimentinα-SMAAmino acid supplements -SMAD3CD68 Health benefits of potassium, CD3 and Troponin I iDsease purchased from Abcam, Disdase.
ECL andd blot detection kits FD were purchased from Heary bio Snd Biological Technology Co. A cell counting kit-8 CCK-8 dye Chrcumin purchased from Biosharp, Inc.
Heaart was obtained from RWD Life Science Ane. Picro Sirius Red Diseasr was obtained from Sbjbio Nanjing SenBeiJia Biological Technology Co.
ELISA kit was used to quantify IL ml Shanghai Enzyme-linked Biotechnology Co. All experiments were approved by the Ethical Committee of Zhejiang University and all surgical procedures were performed by experienced technician sin a blinded manner.
Mice were acclimatized to the standard conditions with 12 h lighting cycle, 25 ± 2°C temperature, free access to water and standard chow for 1 week. Then, they were sorted into four groups of 10 mice per group. Group 1 sham received dimethylsulfoxide DMSO-saline for 28 days intragastrically i.
as a vehicle for curcumin. for 28 days after MI. MI was induced by ligation of the left anterior descending coronary artery. The MI model was established as described previously Hu et al. During 4 weeks treatment, mice was anaesthetized 1.
Two-dimensional B-mode and M-mode measurements in the long-axis view level include left ventricular end-diastolic dimension LVID,dleft ventricular end-systolic dimension LVID,sinterventricular septal wall thickness in diastole IVS,d and in systole IVS,sand left ventricular posterior wall thickness in diastole LVPW,d and in systole LVPW,s.
Left ventricular ejection fraction and fractional shortening were automatically calculated by the echocardiographic system Xiao et al. The sections were then stained with a In Situ Cell Death Detection Kit Roche Applied Science, CHCD3, CD68, Troponin I Abcam, United Kingdomand DAPI Vector Laboratories, Burlingame, CA, United States.
After deparaffinization, sections were stained with Sirius Red. Tissue damage was scored by calculating the scar circumference, including both internal and external scar diameters.
The sirius red—stained sections were scanned with a microscope digital camera Olympus Instrument, United Statesand Biotechnologies, China. The percentage of fibrotic area was calculated as the mean value of the endocardial and epicardial length of the whole fibrotic area in proportion to the mean length of the endocardial and epicardial left ventricle using Image using Image Pro Plus software version 6.
Mouse macrophage-like Raw After 2 days, the medium was replaced, and nonadherent cells were discarded. Following treatment, 10 μL of CCK-8 solution was added to each well and incubated for 2 h.
The absorbance of each well was measured at and nm using a microplate reader Spark TECAN, Switzerland. All data were calculated from triplicate samples. Cell apoptosis was evaluated by flow cytometry with Annexin V-FITC and PI staining CytoFlex, Beckman Coulter, Germany. NRCFs in each group were seeded in a 6-well plate at 2 × 10 5 cells per well and cultured in FBS free medium overnight.
NRCFs were transfected for 48 h with 2 μg of the IL18 mimic IL rat, Shanghai GenePharma Co. Real-time fluorescent quantitative polymerase chain reaction RT-qPCR and enzyme-linked immunosorbent assay ELISA were used to quantify IL transfection efficiency.
And resultant cDNA samples were subjected to qPCR on LightCycler ® PCR System Roche using SYBR ® Green Premix Pro Taq HS qPCR Kit AG.
The upstream and downstream primers of IL6, IL-1β, and TNF-α were designed and synthesized by Tsingke Biotechnology Co. The primer sequences used were as follows:.
The cells seeded in the 6-well plates were collected, lysed in 2. Finally, the immunoreactive protein was detected by a chemiluminescence assay AIRGB, GE HealthCare, United States using the FDbio-Dura ECL kit FDbio Science Biological Technology Co. All results were expressed as value ±standard error of the mean SEM.
Statistical calculations were carried out using GraphPad Prism 9. To test the effect of curcumin on MI, we performed MI surgery by permanent ligation of the left anterior descending artery followed by intragastric administration of curcumin for 7 days or 28 days. In parallel, a placebo post-MI group was also established.
To summarize, the administration of curcumin after MI significantly ameliorated inflammation in the acute phase; however, curcumin exerted a protective effect by preserving long-term cardiac function only after MI, which suggested that the reduced inflammation activation might be related to adverse cardiac remodeling mediated by curcumin intake.
FIGURE 1. Curcumin administration ameliorates inflammatory response in acute phase post-MI and preserves long-term cardiac function A.
Troponins were identified by green coloring; statistical data are summarized in B. Troponins were identified by green coloring; statistical data are summarized in D. Echocardiography were conducted at baseline and 3, 7, 14, and 28 days post-MI.
Left ventricular internal dimension in systolic phase LVID s and Left ventricular internal dimension in diastolic phase LVID d in each group at different timepoint were also plotted in H and I.
MI: myocardial infarction. Results are mean with SEM. As previously indicated, curcumin delivery significantly improved long-term cardiac function after MI in C57 mice.
To determine what yields this beneficial effect, we conducted TUNEL and picro sirius red staining and, surprisingly, discovered no significant reduction in anti-apoptotic effect on cardiomyocyte within border area in the curcumin-treated group compared with the placebo group 7 days after MI Supplementary Figure S1A,B.
However, we observed dramatically reduced scar formation reflected by picro sirius red staining in both scar circumference and infarct size dimension in curcumin group compared with the placebo group Figures 2A—C. The results presented above indicate that the use of curcumin following MI significantly improved cardiac function by inhibiting excessive collagen deposition and scar formation.
FIGURE 2. Curcumin reduces scar formation and ameliorates adverse cardiac remodeling in post-MI rats in long-term prospects A-B. Representative images of sirius red staining of whole heart cross section in rat heart from all groups, as indicated A B Statistical analysis of scar circumference in each group means with SEM.
Collagen summary and statistics are plotted in E F-G. It is known that LPS significantly activate inflammation and mobilize macrophage proliferation as well as M1 polarization. To further investigate the mechanism of curcumin in anti-inflammatory processes, we performed LPS stimulation on macrophage in vitro for 24 h followed by Curcumin administration, CCK8 test revealed dramatic inhibited macrophage proliferation when dosage was 20 uM, indicating Curcumin might exerted anti-proliferation or pro-apoptotic effect in macrophages under LPS stimulation Figure 3A.
Flow cytometry was conducted to determine whether curcumin promoted macrophage apoptosis under LPS stimulation. As shown in Figures 3B,Ccurcumin significantly increased macrophage apoptosis under LPS stimulation compared with LPS only also using 20 uM dosage. In addition, the cleaved-caspase three protein level, which acts as a marker of apoptosis, was also significantly up-regulated in the curcumin-treated macrophages with LPS group compared with LPS only reflected by western blot Figures 3D,E.
Furthermore, macrophage activation could induce the secretion of pro-inflammatory cytokines such as IL-6, IL1β, and TNF-α to initiate an immune response to ischemic injury, thus aggravating cardiomyocyte apoptosis; however, curcumin treatment significantly inhibited pro-inflammatory cytokine secretion in macrophages with LPS group compared with LPS only, as reflected by reduced IL-6, IL-1β, and TNF-α secretion especially at 20 uM concentration Figures 3F—H.
These data indicate that the administration of curcumin on macrophages under LPS stimulation exerted both pro-apoptotic effects in macrophages and anti-inflammatory effects by reducing cytokine release from macrophages, which could be greatly beneficial post-MI.
FIGURE 3. Curcumin promotes macrophage apoptosis in vitro and restrain pro-inflammatory cytokine secretio A. As previously mentioned, curcumin has also been shown to regulate macrophage polarization by increasing anti-inflammatory cytokine IL levels and decreasing the M1 phenotype marker CD86 along with the pro-inflammatory cytokines TNF-α and IL To validate whether curcumin exerted an inhibitory effect on cardiac fibrosis by alleviating inflammation-induced fibrosis or by directly suppressing cardiac fibroblast trans -differentiation and collagen secretion, we co-cultured macrophages under LPS stimulation with isolated primary neonatal rat cardiac fibroblasts in vitro followed by TGF-β stimulation in NRCF for 24 h, Surprisingly, we discovered that curcumin administration in macrophages with LPS stimulation significantly mitigated collagen synthesis from co-cultured NRCF, which was revealed by pro-fibrotic protein expression α-SMA, Vimentin, Periostin, and EDA-Fibronectin Figure 4A,C—F.
In contrast, we did not observe a significant change in fibrosis protein expression when curcumin was directly added to NRCF treated with TGF-β for 24 h compared with the TGF-β only group Figure 4B,G—J.
: Curcumin and Heart Disease| Breadcrumb | Kane GC , Karon BL , Mahoney DW , Redfield MM , Roger VL , Burnett JC , Jacobsen SJ , Rodeheffer RJ. ESC Publications. It involves free radicals, highly reactive molecules with unpaired electrons. Curcumin is a polyphenol found in the spice turmeric that is used as a natural drug. J Diet Suppl ;— |
| 10 Health Benefits of Tumeric and Curcumin | Menon VP , Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol ; : — Morimoto T , Sunagawa Y , Kawamura T , Takaya T , Wada H , Nagasawa A , Komeda M , Fujita M , Shimatsu A , Kita T , Hasegawa K. The dietary compound curcumin inhibits p histone acetyltransferase activity and prevents heart failure in rats. J Clin Invest ; : — Sunagawa Y , Funamoto M , Shimizu K , Shimizu S , Sari N , Katanasaka Y , Miyazaki Y , Kakeya H , Hasegawa K , Morimoto T. Curcumin, an inhibitor of pHAT activity, suppresses the development of hypertension-induced left ventricular hypertrophy with preserved ejection fraction in Dahl rats. Nutrients ; 13 : Sunagawa Y , Morimoto T , Wada H , Takaya T , Katanasaka Y , Kawamura T , Yanagi S , Marui A , Sakata R , Shimatsu A , Kimura T , Kakeya H , Fujita M , Hasegawa K. A natural pspecific histone acetyltransferase inhibitor, curcumin, in addition to angiotensin-converting enzyme inhibitor, exerts beneficial effects on left ventricular systolic function after myocardial infarction in rats. Circ J ; 75 : — Sasaki H , Sunagawa Y , Takahashi K , Imaizumi A , Fukuda H , Hashimoto T , Wada H , Katanasaka Y , Kakeya H , Fujita M , Hasegawa K , Morimoto T. Innovative preparation of curcumin for improved oral bioavailability. Biol Pharm Bull ; 34 : — Sunagawa Y , Wada H , Suzuki H , Sasaki H , Imaizumi A , Fukuda H , Hashimoto T , Katanasaka Y , Shimatsu A , Kimura T , Kakeya H , Fujita M , Hasegawa K , Morimoto T. A novel drug delivery system of oral curcumin markedly improves efficacy of treatment for heart failure after myocardial infarction in rats. Biol Pharm Bull ; 35 : — Solomon SD , McMurray JJV , Anand IS , Ge J , Lam CSP , Maggioni AP , Martinez F , Packer M , Pfeffer MA , Pieske B , Redfield MM , Rouleau JL , van Veldhuisen DJ , Zannad F , Zile MR , Desai AS , Claggett B , Jhund PS , Boytsov SA , Comin-Colet J , Cleland J , Düngen H-D , Goncalvesova E , Katova T , Kerr Saraiva JF , Lelonek M , Merkely B , Senni M , Shah SJ , Zhou J , Rizkala AR , Gong J , Shi VC , Lefkowitz MP. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med ; : — Anker SD , Butler J , Filippatos G , Ferreira JP , Bocchi E , Böhm M , Brunner-La Rocca H-P , Choi D-J , Chopra V , Chuquiure-Valenzuela E , Giannetti N , Gomez-Mesa JE , Janssens S , Januzzi JL , Gonzalez-Juanatey JR , Merkely B , Nicholls SJ , Perrone SV , Piña IL , Ponikowski P , Senni M , Sim D , Spinar J , Squire I , Taddei S , Tsutsui H , Verma S , Vinereanu D , Zhang J , Carson P , Lam CSP , Marx N , Zeller C , Sattar N , Jamal W , Schnaidt S , Schnee JM , Brueckmann M , Pocock SJ , Zannad F , Packer M. Empagliflozin in heart failure with a preserved ejection fraction. Packer M , Zannad F , Anker SD. Heart failure and a preserved ejection fraction: a side-by-side examination of the PARAGON-HF and EMPEROR-Preserved trials. Butler J , Packer M , Filippatos G , Ferreira JP , Zeller C , Schnee J , Brueckmann M , Pocock SJ , Zannad F , Anker SD. Effect of empagliflozin in patients with heart failure across the spectrum of left ventricular ejection fraction. Eur Heart J ; 43 : — Kasiakogias A , Rosei EA , Camafort M , Ehret G , Faconti L , Ferreira JP , Brguljan J , Januszewicz A , Kahan T , Manolis A , Tsioufis K , Weber T , von Lueder TG , Smiseth OA , Wachtell K , Kjeldsen SE , Zannad F , Mancia G , Kreutz R. Hypertension and heart failure with preserved ejection fraction: position paper by the European Society of Hypertension. J Hypertens ; 39 : — Fagard RH , Celis H , Thijs L , Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension ; 54 : — Funamoto M , Sunagawa Y , Katanasaka Y , Miyazaki Y , Imaizumi A , Kakeya H , Yamakage H , Satoh-Asahara N , Komiyama M , Wada H , Hasegawa K , Morimoto T. Highly absorptive curcumin reduces serum atherosclerotic low-density lipoprotein levels in patients with mild COPD. Int J Chron Obstruct Pulmon Dis ; 11 : — Redfield MM , Jacobsen SJ , Burnett JC , Mahoney DW , Bailey KR , Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA ; : — Kane GC , Karon BL , Mahoney DW , Redfield MM , Roger VL , Burnett JC , Jacobsen SJ , Rodeheffer RJ. Progression of left ventricular diastolic dysfunction and risk of heart failure. Maisel AS , Krishnaswamy P , Nowak RM , McCord J , Hollander JE , Duc P , Omland T , Storrow AB , Abraham WT , Wu AHB , Clopton P , Steg PG , Westheim A , Knudsen CW , Perez A , Kazanegra R , Herrmann HC , McCullough PA. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. Redfield MM , Rodeheffer RJ , Jacobsen SJ , Mahoney DW , Bailey KR , Burnett JC. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am Coll Cardiol ; 40 : — Dockery F , Bulpitt CJ , Agarwal S , Vernon C , Nihoyannopoulos P , Kemp M , Hooper J , Rajkumar C. Anti-androgens increase N-terminal pro-BNP levels in men with prostate cancer. Clin Endocrinol Oxf ; 68 : 59 — Saenger AK , Dalenberg DA , Bryant SC , Grebe SK , Jaffe AS. Pediatric brain natriuretic peptide concentrations vary with age and sex and appear to be modulated by testosterone. Clin Chem ; 55 : — Benefits of curcumin in the vasculature: a therapeutic candidate for vascular remodeling in arterial hypertension and pulmonary arterial hypertension. Front Physiol ; 13 : Funamoto M , Sunagawa Y , Katanasaka Y , Shimizu K , Miyazaki Y , Sari N , Shimizu S , Mori K , Wada H , Hasegawa K , Morimoto T. Histone acetylation domains are differentially induced during development of heart failure in dahl salt-sensitive rats. Int J Mol Sci ; 22 : Funamoto M , Shimizu K , Sunagawa Y , Katanasaka Y , Miyazaki Y , Kakeya H , Yamakage H , Satoh-Asahara N , Wada H , Hasegawa K , Morimoto T. Effects of highly absorbable curcumin in patients with impaired glucose tolerance and non-insulin-dependent diabetes mellitus. J Diabetes Res ; : Shimizu K , Funamoto M , Sunagawa Y , Shimizu S , Katanasaka Y , Miyazaki Y , Wada H , Hasegawa K , Morimoto T. Anti-inflammatory action of curcumin and its use in the treatment of lifestyle-related diseases. Eur Cardiol ; 14 : — Altinel Y , Yalçın Ş , Ercan G , Yavuz E , Erçetin C , Gülçiçek OB , Çelik A , Özkaya G , Uzun H. The efficacy of curcumin on PDGF expression and NF-kappa B pathway: TNBS-induced colitis. Ulus Travma Acil Cerrahi Derg ; 26 : — Klingbeil AU , Schneider M , Martus P , Messerli FH , Schmieder RE. A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. Rasyid A , Lelo A. The effect of curcumin and placebo on human gall-bladder function: an ultrasound study. Aliment Pharmacol Ther ; 13 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Advertisement intended for healthcare professionals. Navbar Search Filter European Heart Journal Open This issue ESC Publications Cardiovascular Medicine Books Journals Oxford Academic Mobile Enter search term Search. ESC Publications. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume 2. Article Contents Abstract. Lead author biography. Data Availability. Supplementary material. Journal Article. Effects of high-absorption curcumin for the prevention of hypertensive heart disease: a double-blind, placebo-controlled, randomized clinical study. Masafumi Funamoto , Masafumi Funamoto. Division of Translational Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center. Division of Molecular Medicine, School of Pharmaceutical Sciences, University of Shizuoka. Department of Pharmacology, Institute of Biomedical Sciences, Tokushima University Graduate School. Oxford Academic. Yoichi Sunagawa. Yasufumi Katanasaka. Toru Kato. Department of Clinical Research, National Hospital Organization Tochigi Medical Center. Junichi Funada. Department of Cardiology, National Hospital Organization Ehime Medical Center. Yoichi Ajiro. Division of Clinical Research, National Hospital Organization Yokohama Medical Center. Maki Komiyama. Masaharu Akao. Akihiro Yasoda. Hajime Yamakage. Noriko Satoh-Asahara , Noriko Satoh-Asahara. Hiromichi Wada. Yasumasa Ikeda. Tatsuya Morimoto. Koji Hasegawa. Corresponding author. It is also used in mustard and to color butter and cheese. Turmeric has been used in both Ayurvedic and Chinese medicine as an anti-inflammatory, to treat digestive and liver problems, skin diseases, and wounds. Curcumin is also a powerful antioxidant. Antioxidants scavenge molecules in the body known as free radicals, which damage cell membranes, tamper with DNA, and even cause cell death. Antioxidants can fight free radicals and may reduce or even help prevent some of the damage they cause. In addition, curcumin lowers the levels of two enzymes in the body that cause inflammation. It also stops platelets from clumping together to form blood clots. Curcumin stimulates the gallbladder to produce bile, which some people think may help improve digestion. The German Commission E, which determines which herbs can be safely prescribed in Germany, has approved turmeric for digestive problems. And one double-blind, placebo-controlled study found that turmeric reduced symptoms of bloating and gas in people suffering from indigestion. Turmeric may help people with ulcerative colitis stay in remission. Ulcerative colitis is a chronic disease of the digestive tract where symptoms tend to come and go. In one double-blind, placebo-controlled study, people whose ulcerative colitis was in remission took either curcumin or placebo, along with conventional medical treatment, for 6 months. Those who took curcumin had a significantly lower relapse rate than those who took placebo. Turmeric does not seem to help treat stomach ulcers. In fact, there is some evidence that it may increase stomach acid, making existing ulcers worse. See "Precautions" section. Because of turmeric's ability to reduce inflammation, researchers have wondered if it may help relieve osteoarthritis pain. One study found that people using an Ayurvedic formula of herbs and minerals with turmeric, winter cherry Withinia somnifera , boswellia Boswellia serrata , and zinc had less pain and disability. But it's impossible to know whether turmeric, one of the other supplements, or all of them together, was responsible for the effects. Early studies suggested that turmeric may help prevent atherosclerosis, the buildup of plaque that can block arteries and lead to heart attack or stroke. In animal studies, an extract of turmeric lowered cholesterol levels and kept LDL bad cholesterol from building up in blood vessels. Because it stops platelets from clumping together, turmeric may also prevent blood clots from building up along the walls of arteries. But a double-blind, placebo-controlled study found that taking curcumin, the active ingredient in turmeric, at a dose of up to 4 g per day did not improve cholesterol levels. There has been a great deal of research on turmeric's anti-cancer properties, but results are still preliminary. Evidence from test tube and animal studies suggests that curcumin may help prevent or treat several types of cancers, including prostate, breast, skin, and colon cancer. Tumeric's preventive effects may relate to its antioxidant properties, which protect cells from damage. More research is needed. Cancer should be treated with conventional medications. Don't use alternative therapies alone to treat cancer. If you choose to use complementary therapies along with your cancer treatment, make sure you tell all your doctors. Test tube and animal studies suggest turmeric may kill bacteria and viruses, but researchers don't know whether it would work in people. A preliminary study suggests curcumin may help treat uveitis, an inflammation of the eye's iris. Preliminary research suggests that curcumin may be as effective as corticosteroids, the type of medication usually prescribed. Tumeric's powerful antioxidant, anti-inflammatory, and circulatory effects may help prevent and treat neurodegenerative diseases, including Alzheimer disease, Parkinson's disease, multiple sclerosis, and other conditions. A relative of ginger, turmeric is a perennial plant that grows 5 to 6 feet high in the tropical regions of Southern Asia, with trumpet-shaped, dull yellow flowers. Its roots are bulbs that also produce rhizomes, which then produce stems and roots for new plants. Turmeric is fragrant and has a bitter, somewhat sharp taste. Although it grows in many tropical locations, the majority of turmeric is grown in India, where it is used as a main ingredient in curry. The roots, or rhizomes and bulbs, are used in medicine and food. They are generally boiled and then dried, turning into the familiar yellow powder. Curcumin, the active ingredient, has antioxidant properties. Other substances in this herb have antioxidant properties as well. Bromelain increases the absorption and anti-inflammatory effects of curcumin, so it is often combined with turmeric products. Pediatric Turmeric supplements haven't been studied in children, so there is no recommended dose. The use of herbs is a time-honored approach to strengthening the body and treating disease. However, herbs can trigger side effects and may interact with other herbs, supplements, or medications. For these reasons, you should take herbs with care, under the supervision of a health care provider. Turmeric in food is considered safe. However, taking large amounts of turmeric and curcumin in supplement form for long periods of time may cause stomach upset and, in extreme cases, ulcers. People who have gallstones or obstruction of the bile passages should talk to their doctor before taking turmeric. If you have diabetes, talk to your doctor before taking turmeric supplements. Turmeric may lower blood sugar levels. When combined with medications for diabetes, turmeric could cause hypoglycemia low blood sugar. Although it is safe to eat foods with turmeric, pregnant and breastfeeding women should not take turmeric supplements. Because turmeric may act like a blood thinner, you should stop taking it at least 2 weeks before surgery. Tell your doctor and surgeon that you have been taking turmeric. If you are being treated with any of the following medications, you should not use turmeric or curcumin in medicinal forms without first talking to your health care provider. Turmeric may strengthen the effects of these drugs, raising the risk of bleeding. Blood thinners include warfarin Coumadin , clopidogrel Plavix , and aspirin, among others. Turmeric may interfere with the action of these drugs, increasing the production of stomach acid:. Turmeric may strengthen the effects of these drugs, increasing the risk of hypoglycemia low blood sugar. Aggarwal BB, Yuan W, Li S, Gupta SC. Curcumin-free tumeric exhibits anti-inflammatory and anticancer activities: Identification of novel components of tumeric. Mol Nutr Food Res. Pharm Biol. Li ZY, Ding LL, Li JM, Xu BL, Yang L, Bi KS, Wang ZT. PLoS One. Article PubMed PubMed Central Google Scholar. Shin SK, Ha TY, McGregor RA, Choi MS. Long-term curcumin administration protects against atherosclerosis via hepatic regulation of lipoprotein cholesterol metabolism. Mol Nutr Food Res. Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N. Effect of NCB, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study. Drugs R D. Soni KB, Kuttan R. Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian J Physiol Pharmacol. CAS PubMed Google Scholar. Ramirez-Bosca A, Soler A, Carrion MA, Diaz-Alperi J, Bernd A, Quintanilla C, Quintanilla Almagro E, Miquel J. Implications for atherogenesis prevention. Mech Ageing Dev. Pungcharoenkul K, Thongnopnua P. Effect of different curcuminoid supplement dosages on total in vivo antioxidant capacity and cholesterol levels of healthy human subjects. Phytother Res. Mohammadi A, Sahebkar A, Iranshahi M, Amini M, Khojasteh R, Ghayour-Mobarhan M, Ferns GA. Effects of supplementation with curcuminoids on dyslipidemia in obese patients: a randomized crossover trial. Baum L, Cheung SK, Mok VC, Lam LC, Leung VP, Hui E, Ng CC, Chow M, Ho PC, Lam S, et al. Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol Res. Alwi I, Santoso T, Suyono S, Sutrisna B, Suyatna FD, Kresno SB, Ernie S. The effect of curcumin on lipid level in patients with acute coronary syndrome. Acta Med Indones. PubMed Google Scholar. A systematic review and meta-analysis of randomized controlled trials investigating the effects of curcumin on blood lipid levels. Clin Nutr. Rahmani S, Asgary S, Askari G, Keshvari M, Hatamipour M, Feizi A, Sahebkar A. Treatment of non-alcoholic fatty liver disease with Curcumin: a randomized placebo-controlled trial. Rahimi HR, Mohammadpour AH, Dastani M, Jaafari MR, Abnous K, Ghayour Mobarhan M, Kazemi OR. The effect of nano-curcumin on HbA1c, fasting blood glucose, and lipid profile in diabetic subjects: a randomized clinical trial. Avicenna J Phytomed. PubMed PubMed Central Google Scholar. Maithili Karpaga Selvi N, Sridhar MG, Swaminathan RP, Sripradha R. Efficacy of turmeric as adjuvant therapy in type 2 diabetic patients. Indian J Clin Biochem. Amin F, Islam N, Anila N, Gilani AH. Clinical efficacy of the co-administration of turmeric and black seeds Kalongi in metabolic syndrome - a double blind randomized controlled trial - TAK-MetS trial. Complement Ther Med. Yang YS, Su YF, Yang HW, Lee YH, Chou JI, Ueng KC. Lipid-lowering effects of curcumin in patients with metabolic syndrome: a randomized, double-blind, placebo-controlled trial. Chuengsamarn S, Rattanamongkolgul S, Phonrat B, Tungtrongchitr R, Jirawatnotai S. Reduction of atherogenic risk in patients with type 2 diabetes by curcuminoid extract: a randomized controlled trial. J Nutr Biochem. Daily JW, Yang M, Park S. Efficacy of turmeric extracts and Curcumin for alleviating the symptoms of joint arthritis: a systematic review and meta-analysis of randomized clinical trials. J Med Food. Higgins JP, Altman DG, Gotzsche PC, Juni P, Moher D, Oxman AD, Savovic J, Schulz KF, Weeks L, Sterne JA, et al. The Cochrane Collaboration's tool for assessing risk of bias in randomised trials. Higgins JPT, Green S, editors. Cochrane handbook for systematic reviews of interventions version 5. The Cochrane Collaboration; Hozo SP, Djulbegovic B, Hozo I. Estimating the mean and variance from the median, range, and the size of a sample. BMC Med Res Methodol. Panahi Y, Khalili N, Hosseini MS, Abbasinazari M, Sahebkar A. Lipid-modifying effects of adjunctive therapy with curcuminoids-piperine combination in patients with metabolic syndrome: results of a randomized controlled trial. Sahebkar A, Mohammadi A, Atabati A, Rahiman S, Tavallaie S, Iranshahi M, Akhlaghi S, Ferns GA, Ghayour-Mobarhan M. Curcuminoids modulate pro-oxidant-antioxidant balance but not the immune response to heat shock protein 27 and oxidized LDL in obese individuals. Panahi Y, Hosseini MS, Khalili N, Naimi E, Soflaei SS, Majeed M, Sahebkar A. Effects of supplementation with curcumin on serum adipokine concentrations: a randomized controlled trial. Panahi Y, Hosseini MS, Khalili N, Naimi E, Simental-Mendia LE, Majeed M, Sahebkar A. Effects of curcumin on serum cytokine concentrations in subjects with metabolic syndrome: a post-hoc analysis of a randomized controlled trial. Biomed Pharmacother. Heinl RE, Dhindsa DS, Mahlof EN, Schultz WM, Ricketts JC, Varghese T, Esmaeeli A, Allard-Ratick MP, Millard AJ, Kelli HM, et al. Comprehensive cardiovascular risk reduction and cardiac rehabilitation in diabetes and the metabolic syndrome. Can J Cardiol. Brede S, Serfling G, Klement J, Schmid SM, Lehnert H. Clinical scenario of the metabolic syndrome. Visc Med. Anand P, Kunnumakkara AB, Newman RA, Aggarwal BB. Bioavailability of curcumin: problems and promises. Mol Pharm. Murdande SB, Pikal MJ, Shanker RM, Bogner RH. Aqueous solubility of crystalline and amorphous drugs: challenges in measurement. Pharm Dev Technol. Mirzabeigi P, Mohammadpour AH, Salarifar M, Gholami K, Mojtahedzadeh M, Javadi MR. The effect of Curcumin on some of traditional and non-traditional cardiovascular risk factors: a pilot randomized, double-blind, Placebo-controlled Trial. Iran J Pharm Res. CAS PubMed PubMed Central Google Scholar. Soare A, Weiss EP, Holloszy JO, Fontana L. Multiple dietary supplements do not affect metabolic and cardio-vascular health. Aging Albany NY. Article Google Scholar. Neerati P, Devde R, Gangi AK. Evaluation of the effect of curcumin capsules on glyburide therapy in patients with type-2 diabetes mellitus. Jayakumar V, Ahmed SS, Ebenezar KK. Multivariate analysis and molecular interaction of curcumin with PPARgamma in high fructose diet induced insulin resistance in rats. Nishiyama T, Mae T, Kishida H, Tsukagawa M, Mimaki Y, Kuroda M, Sashida Y, Takahashi K, Kawada T, Nakagawa K, Kitahara M. Curcuminoids and sesquiterpenoids in turmeric Curcuma Longa L. suppress an increase in blood glucose level in type 2 diabetic KK-ay mice. J Agric Food Chem. Kang Q, Chen A. Curcumin suppresses expression of low-density lipoprotein LDL receptor, leading to the inhibition of LDL-induced activation of hepatic stellate cells. Are curcuminoids effective C-reactive protein-lowering agents in clinical practice? Evidence from a meta-analysis. Curcuminoids for the management of hypertriglyceridaemia. Nat Rev Cardiol. Low-density lipoprotein is a potential target for curcumin: novel mechanistic insights. Basic Clin Pharmacol Toxicol. Sahebkar A, Chew GT, Watts GF. Recent advances in pharmacotherapy for hypertriglyceridemia. Prog Lipid Res. Panahi Y, Ahmadi Y, Teymouri M, Johnston TP, Sahebkar A. Curcumin as a potential candidate for treating hyperlipidemia: a review of cellular and metabolic mechanisms. J Cell Physiol. Cheng AL, Hsu CH, Lin JK, Hsu MM, Ho YF, Shen TS, Ko JY, Lin JT, Lin BR, Ming-Shiang W, et al. Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions. Anticancer Res. Download references. This research was supported by the Natural Science Foundation of China grant no. The funding bodies had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. The tables and figures supporting the conclusions of this article are included within the article. There are also two supplementary tables online. Department of Clinical Nutrition, The Second Affiliated Hospital of Chongqing Medical University, No. You can also search for this author in PubMed Google Scholar. SQ, HR and HDH contributed to the conception and design of the study. SQ, LFH and HDH conducted the literature search and data extraction. LFH and SQ performed the statistical analyses. SQ, LFH, JJG, SSS, JH and HDH drafted the manuscript. HR and HDH supervised the study. All authors gave final approval. Correspondence to Huaidong Hu. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Qin, S. |
| Turmeric Information | Mount Sinai - New York | The onset of remarkable cardiac hypertrophy is rare at the beginning of LV hypertrophy. Venous blood in a fasting state was collected from the cutaneous vein of the forearm by the investigator before, 12 weeks after, and 24 weeks after administration of the test meals. Specifically, the lower limit of the one-sided confidence interval CI; confidence coefficient: 0. The upper limit of the one-sided CI confidence coefficient: 0. We estimated that we would need to enrol patients in the high-absorption curcumin group and placebo group to have 0. We then included patients patients in each group to account for the dropout rate. Comparing data between the two groups, parametric and non-parametric data were analysed using the non-paired t -test and Mann—Whitney U test, respectively. Absolute values in each parameter at baseline and 6 months after initiating treatment were compared using the paired t -test for parametric data and Wilcoxon signed-rank test for non-parametric data. All statistical analyses were performed using SPSS version Patient enrolment for the study was concluded in March Even though the target patient sample size was not achieved, the study period was not extended. This was a result of a delay in patient enrolment and limitations of the research grant. Of the patients enrolled, the following patients were excluded: six patients in the placebo group [withdrawal of consent five patients and discontinuation of treatment by themselves one patient ] and three patients in the high-absorption curcumin group [discontinuation of treatment by themselves two patients and deemed unfit as a subject by the primary physician one patient ]. Therefore, a total of patients were included in this study. During the follow-up period, 2 patients in the high-absorption curcumin group discontinued treatment because of adverse events; therefore, patients completed the follow-up period Figure 1. Echocardiography data and plasma BNP levels were obtained 6 months after study entry, and analyses were performed. There were 69 patients in the placebo group [56 male and 13 female patients with a mean age of Table 1 shows the baseline patient characteristics of the two groups. No differences in the following parameters were observed between the two groups: sex, age, body mass index BMI , systolic blood pressure, diastolic blood pressure, pulse, plasma BNP levels, echocardiography e. left axis deviation, LV end-diastolic diameter, EF, IVS, and PWT , and Doppler echocardiography e. Baseline characteristics of the participants in the placebo and curcumin groups. BMI, body mass index; BNP, brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; Cre, creatinine; DBP, diastolic blood pressure; DcT, deceleration time; EF, ejection fraction; IVS, interventricular septum; LAD, left axis deviation; LVDd, left ventricular end-diastolic diameter; PWT, posterior LV wall thickness; SBP, systolic blood pressure. Table 2 shows the percentage change in each parameter from baseline to 6 months after treatment initiation in the two groups. The percentage change in systolic blood pressure was significantly lower in the high-absorption curcumin group than in the placebo group. The percentage change in plasma BNP levels was significantly lower in the high-absorption curcumin group than in the placebo group. Abbreviations used in this table are the same as in Table 1. After stratification, no significant difference was found in the per cent change in the plasma BNP levels between the placebo and high-absorption groups. In addition, no significant difference was noted in the effects of increased absorption of curcumin between the two groups. Per cent change in brain natriuretic peptide divided by baseline age in each group. Bold line indicates the median and lower and upper lines of the box indicate the lower and upper quartiles, respectively. Per cent change in brain natriuretic peptide divided by baseline value in each group. Supplementary material online , Table S2 shows the baseline data for the placebo group and high-absorption curcumin groups after stratification. The per cent changes in plasma BNP levels and systolic blood pressure were significantly lower in the high-absorption curcumin group than in the placebo group. Two patients in the high-absorption curcumin group discontinued the treatment because of adverse events. Specifically, one patient was hospitalized due to epididymitis, but the patient had a history of this disease; thus, this adverse event was assessed as unrelated to the study meal. The other patient discontinued treatment because of mild adverse events soft stools and heartburn. The relationship between these adverse events and study meal high-absorption curcumin was unknown. However, this patient likely had diarrhoea as blood test results, including liver enzymes, renal function, and blood cells, were unremarkable. This study aimed to examine whether a high-absorption curcumin agent possesses preventable effects in addition to blood pressure control. The percentage change in plasma BNP levels from baseline to 6 months after initiating treatment was significantly lower in the high-absorption curcumin group than in the placebo group. Blood pressure control is the first priority to prevent the future development of HFpEF in patients with hypertension. The results of this study might provide a novel strategy in addition to blood pressure control for the prevention of HFpEF development in the future. However, long-term studies are needed to examine this hypothesis. Brain natriuretic peptide is a hormone secreted primarily by the LV in response to increased cardiac wall stretching and stress. Blood BNP levels increase sharply when a load is exerted on the LV. Due to these characteristics, BNP levels have been widely used as indicators for heart failure diagnosis. This increase may be attributed to the presence of hypertensive cardiac hypertrophy and spontaneous increase with age. Curcumin has been reported to exhibit vasodilating effects through the following possible mechanisms: i inhibition of angiotensin-converting enzyme via nuclear factor-kappa B activation and ii nitric oxide production via endothelial nitric oxide synthase activation. Therefore, the improvement in peripheral circulation by curcumin may be associated with the inhibition of an increase in BNP levels in patients with hypertension. Moreover, our previous study demonstrated that curcumin reduced phenylephrine-induced BNP mRNA levels in cultured cardiomyocyte hypertrophy. We believe that the mechanism of curcumin-induced suppression of blood BNP levels in these patients may be associated with inhibition of BNP expression in the myocardium. In addition to the suppression of myocardial pathological growth, curcumin possesses various bioactive effects, such as anti-inflammatory inhibiting nuclear factor-kappa B , anti-growth antagonizing platelet-derived growth factor , and antioxidant actions scavenging reactive oxygen species, inhibiting lipid peroxidation. In fact, many patients with HFpEF have complications such as diabetes, hypertension, and obesity, which cause systemic inflammatory and oxidative stress. This study did not evaluate an inflammatory marker; however, previous studies that used the same high-absorption curcumin agent have shown that this drug reduces oxidized low-density lipoprotein. It is well known that compliance of the heart and blood vessels decreases with aging. Once age-related phenomena such as calcification and fibrosis occur in the cardiovascular system, it is difficult to completely restore them with drug interventions. This study is the first to examine the cardiac effects of high-absorption curcumin in a double-blind, randomized controlled trial. Currently, the precise mechanisms that explain the lack of curcumin-induced reduction in BNP levels in elderly patients are unclear. Further studies are needed to clarify these mechanisms. Curcumin did not significantly affect the echocardiographic parameters. Generally, changes in blood BNP levels are more sensitive to drug interventions compared with echocardiographic parameters. One patient in the high-absorption curcumin group developed mild adverse events soft stools and heart burn. A previous study using the same high-absorption curcumin agent reported the occurrence of soft stools. Curcumin is a less soluble compound and this may be the cause of the soft stools. Further studies are required to evaluate the relationship between curcumin and soft stool. This study has some limitations. First, the sample size of this study was small, and the follow-up period was 6 months. The endpoint was an examination index i. plasma BNP levels , not death or hospitalization due to heart failure. To examine whether a high-absorption curcumin agent prevents future onset of HFpEF in patients with hypertensive heart disease, a large and long-term study is needed. Moreover, this study included patients exhibiting initial signs of hypertensive heart disease, which was diagnosed based on echocardiographic findings. Therefore, plasma BNP levels were normal or only minimally elevated in these patients. Further studies are required to evaluate whether curcumin improves the prognosis of HFpEF patients. This effect was apparent in non-elderly individuals aged 65 years. The P -values for the interactions and subgroups were not adjusted for multiple testing, and therefore, the reported age-based differences should be viewed as hypothesis-generating only. Further long-term studies are needed to clarify whether a high-absorption curcumin agent will prevent future HFpEF development in this patient population. Koji Hasegawa, MD, PhD, is currently, Director at Division of Translational Research in National Hospital Organization NHO Kyoto Medical Center and Leader of NHO Cardiovascular Clinical Research Network. He is also serving as Clinical Professor, Faculty of Medicine, at Kyoto University as well as Visiting Professor at the University of Shizuoka. He has been widely involved in the study of cardiology, covering areas ranging from prevention to intervention and from translational science to clinical medicine. Professor Koji Hasegawa is internationally active as an executive board director at the International Society of Cardiovascular Pharmacotherapy ISCP and a member of the Tobacco Expert Group at the World Heart Federation WHF. The data that support the findings of this study are available from the corresponding author K. upon reasonable request. Supplementary material is available at European Heart Journal Open online. The authors wish to sincerely thank and acknowledge the individuals who helped to facilitate this study, including clinical research coordinators. This work was supported in part by a Grant-in-Aid for Clinical Research from the National Hospital Organization. Conflict of interest: The Theravalues Corporation markets highly absorbable curcumin Theracurmin®. There is a joint research agreement related to this study between Theravalues and the National Hospital Organization of the Kyoto Medical Center. McDonagh TA , Metra M , Adamo M , Gardner RS , Baumbach A , Böhm M , Burri H , Butler J , Čelutkienė J , Chioncel O , Cleland JGF , Coats AJS , Crespo-Leiro MG , Farmakis D , Gilard M , Heymans S , Hoes AW , Jaarsma T , Jankowska EA , Lainscak M , Lam CSP , Lyon AR , McMurray JJV , Mebazaa A , Mindham R , Muneretto C , Francesco Piepoli M , Price S , Rosano GMC , Ruschitzka F , Kathrine Skibelund A ; ESC Scientific Document Group. Eur Heart J ; 42 : — Google Scholar. Maddox TM , Januzzi JL , Allen LA , Breathett K , Butler J , Davis LL , Fonarow GC , Ibrahim NE , Lindenfeld JA , Masoudi FA , Motiwala SR , Oliveros E , Patterson JH , Walsh MN , Wasserman A , Yancy CW , Youmans QR. J Am Coll Cardiol ; 77 : — Yanazume T , Hasegawa K , Morimoto T , Kawamura T , Wada H , Matsumori A , Kawase Y , Hirai M , Kita T. Cardiac p is involved in myocyte growth with decompensated heart failure. Mol Cell Biol ; 23 : — Miyamoto S , Kawamura T , Morimoto T , Ono K , Wada H , Kawase Y , Matsumori A , Nishio R , Kita T , Hasegawa K. Histone acetyltransferase activity of p is required for the promotion of left ventricular remodeling after myocardial infarction in adult mice in vivo. Circulation ; : — Menon VP , Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol ; : — Morimoto T , Sunagawa Y , Kawamura T , Takaya T , Wada H , Nagasawa A , Komeda M , Fujita M , Shimatsu A , Kita T , Hasegawa K. The dietary compound curcumin inhibits p histone acetyltransferase activity and prevents heart failure in rats. J Clin Invest ; : — Sunagawa Y , Funamoto M , Shimizu K , Shimizu S , Sari N , Katanasaka Y , Miyazaki Y , Kakeya H , Hasegawa K , Morimoto T. Curcumin, an inhibitor of pHAT activity, suppresses the development of hypertension-induced left ventricular hypertrophy with preserved ejection fraction in Dahl rats. Nutrients ; 13 : Sunagawa Y , Morimoto T , Wada H , Takaya T , Katanasaka Y , Kawamura T , Yanagi S , Marui A , Sakata R , Shimatsu A , Kimura T , Kakeya H , Fujita M , Hasegawa K. A natural pspecific histone acetyltransferase inhibitor, curcumin, in addition to angiotensin-converting enzyme inhibitor, exerts beneficial effects on left ventricular systolic function after myocardial infarction in rats. Circ J ; 75 : — Sasaki H , Sunagawa Y , Takahashi K , Imaizumi A , Fukuda H , Hashimoto T , Wada H , Katanasaka Y , Kakeya H , Fujita M , Hasegawa K , Morimoto T. Innovative preparation of curcumin for improved oral bioavailability. Biol Pharm Bull ; 34 : — Sunagawa Y , Wada H , Suzuki H , Sasaki H , Imaizumi A , Fukuda H , Hashimoto T , Katanasaka Y , Shimatsu A , Kimura T , Kakeya H , Fujita M , Hasegawa K , Morimoto T. A novel drug delivery system of oral curcumin markedly improves efficacy of treatment for heart failure after myocardial infarction in rats. Biol Pharm Bull ; 35 : — Solomon SD , McMurray JJV , Anand IS , Ge J , Lam CSP , Maggioni AP , Martinez F , Packer M , Pfeffer MA , Pieske B , Redfield MM , Rouleau JL , van Veldhuisen DJ , Zannad F , Zile MR , Desai AS , Claggett B , Jhund PS , Boytsov SA , Comin-Colet J , Cleland J , Düngen H-D , Goncalvesova E , Katova T , Kerr Saraiva JF , Lelonek M , Merkely B , Senni M , Shah SJ , Zhou J , Rizkala AR , Gong J , Shi VC , Lefkowitz MP. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med ; : — Anker SD , Butler J , Filippatos G , Ferreira JP , Bocchi E , Böhm M , Brunner-La Rocca H-P , Choi D-J , Chopra V , Chuquiure-Valenzuela E , Giannetti N , Gomez-Mesa JE , Janssens S , Januzzi JL , Gonzalez-Juanatey JR , Merkely B , Nicholls SJ , Perrone SV , Piña IL , Ponikowski P , Senni M , Sim D , Spinar J , Squire I , Taddei S , Tsutsui H , Verma S , Vinereanu D , Zhang J , Carson P , Lam CSP , Marx N , Zeller C , Sattar N , Jamal W , Schnaidt S , Schnee JM , Brueckmann M , Pocock SJ , Zannad F , Packer M. Empagliflozin in heart failure with a preserved ejection fraction. Packer M , Zannad F , Anker SD. Heart failure and a preserved ejection fraction: a side-by-side examination of the PARAGON-HF and EMPEROR-Preserved trials. Butler J , Packer M , Filippatos G , Ferreira JP , Zeller C , Schnee J , Brueckmann M , Pocock SJ , Zannad F , Anker SD. Effect of empagliflozin in patients with heart failure across the spectrum of left ventricular ejection fraction. Eur Heart J ; 43 : — Kasiakogias A , Rosei EA , Camafort M , Ehret G , Faconti L , Ferreira JP , Brguljan J , Januszewicz A , Kahan T , Manolis A , Tsioufis K , Weber T , von Lueder TG , Smiseth OA , Wachtell K , Kjeldsen SE , Zannad F , Mancia G , Kreutz R. Hypertension and heart failure with preserved ejection fraction: position paper by the European Society of Hypertension. J Hypertens ; 39 : — Fagard RH , Celis H , Thijs L , Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension ; 54 : — Funamoto M , Sunagawa Y , Katanasaka Y , Miyazaki Y , Imaizumi A , Kakeya H , Yamakage H , Satoh-Asahara N , Komiyama M , Wada H , Hasegawa K , Morimoto T. Highly absorptive curcumin reduces serum atherosclerotic low-density lipoprotein levels in patients with mild COPD. Int J Chron Obstruct Pulmon Dis ; 11 : — Redfield MM , Jacobsen SJ , Burnett JC , Mahoney DW , Bailey KR , Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA ; : — Kane GC , Karon BL , Mahoney DW , Redfield MM , Roger VL , Burnett JC , Jacobsen SJ , Rodeheffer RJ. Progression of left ventricular diastolic dysfunction and risk of heart failure. Maisel AS , Krishnaswamy P , Nowak RM , McCord J , Hollander JE , Duc P , Omland T , Storrow AB , Abraham WT , Wu AHB , Clopton P , Steg PG , Westheim A , Knudsen CW , Perez A , Kazanegra R , Herrmann HC , McCullough PA. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. Redfield MM , Rodeheffer RJ , Jacobsen SJ , Mahoney DW , Bailey KR , Burnett JC. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am Coll Cardiol ; 40 : — Dockery F , Bulpitt CJ , Agarwal S , Vernon C , Nihoyannopoulos P , Kemp M , Hooper J , Rajkumar C. Anti-androgens increase N-terminal pro-BNP levels in men with prostate cancer. Clin Endocrinol Oxf ; 68 : 59 — Saenger AK , Dalenberg DA , Bryant SC , Grebe SK , Jaffe AS. Pediatric brain natriuretic peptide concentrations vary with age and sex and appear to be modulated by testosterone. Clin Chem ; 55 : — Benefits of curcumin in the vasculature: a therapeutic candidate for vascular remodeling in arterial hypertension and pulmonary arterial hypertension. Front Physiol ; 13 : Funamoto M , Sunagawa Y , Katanasaka Y , Shimizu K , Miyazaki Y , Sari N , Shimizu S , Mori K , Wada H , Hasegawa K , Morimoto T. Histone acetylation domains are differentially induced during development of heart failure in dahl salt-sensitive rats. Int J Mol Sci ; 22 : Funamoto M , Shimizu K , Sunagawa Y , Katanasaka Y , Miyazaki Y , Kakeya H , Yamakage H , Satoh-Asahara N , Wada H , Hasegawa K , Morimoto T. Effects of highly absorbable curcumin in patients with impaired glucose tolerance and non-insulin-dependent diabetes mellitus. J Diabetes Res ; : Shimizu K , Funamoto M , Sunagawa Y , Shimizu S , Katanasaka Y , Miyazaki Y , Wada H , Hasegawa K , Morimoto T. Anti-inflammatory action of curcumin and its use in the treatment of lifestyle-related diseases. Eur Cardiol ; 14 : — Altinel Y , Yalçın Ş , Ercan G , Yavuz E , Erçetin C , Gülçiçek OB , Çelik A , Özkaya G , Uzun H. The efficacy of curcumin on PDGF expression and NF-kappa B pathway: TNBS-induced colitis. Ulus Travma Acil Cerrahi Derg ; 26 : — Klingbeil AU , Schneider M , Martus P , Messerli FH , Schmieder RE. A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. Rasyid A , Lelo A. Both animal and human studies have found that curcumin may increase brain levels of BDNF. By doing this, it may be effective in delaying or even reversing many brain diseases and age-related decreases in brain function. It may also help improve memory and attention , which seems logical given its effects on BDNF levels. However, more studies are needed to confirm this. Heart disease is the number one cause of death in the world. Research suggests that curcumin may help protect against many steps in the heart disease process. Specifically, it helps improve the function of the endothelium or the lining of your blood vessels. Endothelial dysfunction is a major driver of heart disease. This is when your endothelium is unable to regulate blood pressure, blood clotting, and various other factors. Several other studies also suggest that curcumin can lead to improvements in heart health. In addition, curcumin can help reduce inflammation and oxidation as discussed above , which can play a role in heart disease. Many different forms of cancer appear to be affected by curcumin supplements. In fact, curcumin has been studied as a beneficial herb in cancer treatment and has been found to affect cancer growth and development. Studies have shown that it can:. There is also evidence that curcumin may prevent cancer from occurring in the first place, especially cancers of the digestive system like colorectal cancer. In addition, research suggests that curcumin can help clear the buildup of protein tangles called amyloid plaques that are caused by the disease. There are several different types of arthritis , most of which involve inflammation in the joints. In a study on people with osteoarthritis, curcumin appeared to be more effective in relieving pain than a placebo, and research has also found its effect to be similar to that of non-steroidal anti-inflammatory drugs NSAIDs. In another study on rheumatoid arthritis, curcumin appeared to have helped reduce disease-related inflammation. That said, more study is needed to understand if curcumin can actually replace such drugs as a treatment for arthritis inflammation pain. Curcumin has shown some promise in treating mood disorders. Its positive effects on the brain include boosting the brain neurotransmitters serotonin and dopamine, reducing inflammation, and encouraging brain plasticity. This suggests the herb may be an effective antidepressant. Depression is also linked to reduced levels of BDNF and a shrinking hippocampus, a brain area with a role in learning and memory. Curcumin can help boost BDNF levels , potentially reversing some of these changes. A animal study also found that curcumin may help reduce anxiety, though studies on humans are needed to verify this. Given that oxidation and inflammation are believed to play a role in aging, curcumin may have effects that go way beyond just preventing disease. If you stick to 12 g or less , you are not likely to experience side effects such as diarrhea, constipation, or vomiting. Learn more about turmeric dosage. People who are pregnant or nursing, people who have gallbladder or kidney problems, those with bleeding disorders, diabetes, or iron deficiency should limit turmeric. If you have any of these conditions, ask your doctor before taking turmeric. There is research suggesting that curcumin, the main component of turmeric, might help with reducing belly fat. Learn more: Does turmeric help you lose weight? It may also help improve symptoms of depression and arthritis. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Certain herbs and spices are known to have anti-inflammatory properties. Learn about the power of turmeric, ginger, cinnamon, garlic, cayenne, cloves…. Turmeric contains many plant substances, but curcumin is the most powerful. This article looks at the benefits of and key differences between turmeric…. Learn about turmeric tea benefits, who should drink it, and how to make it at home. Golden milk — also known as turmeric milk — is a hot Indian drink made with milk and various spices. Here are 10 science-based benefits of golden milk…. For hundreds of years, people around the world have been using turmeric for its healing properties and cosmetic benefits. Research shows that it's a…. Phosphatidylcholine is known to boost cognition, but its potential benefits don't stop there. Here's what you should know about this herbal remedy. Research suggests rhodiola and ashwagandha work well together, but you may want to take them at different times of day. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based 10 Health Benefits of Tumeric and Curcumin. Medically reviewed by Imashi Fernando, MS, RDN, CDCES — By Kris Gunnars, BSc — Updated on November 27, What it is Medicinal properties Anti-inflammatory Antioxidants Brain health Heart disease Cancer Alzheimer's disease Arthritis Depression Aging FAQs Bottom line Many high-quality studies show that turmeric has major benefits for your body and brain. What are turmeric and curcumin? Turmeric contains bioactive compounds with medicinal properties. |
Curcumin protects against atherosclerosis in apolipoprotein E-knockout mice by inhibiting toll-like receptor 4 expression. J Agric Food Chem ;— Crossref PubMed Ghosh SS, Righi S, Krieg R, et al. High fat high cholesterol diet Western diet aggravates atherosclerosis, hyperglycemia and renal failure in nephrectomized LDL receptor knockout mice: role of intestine derived lipopolysaccharide. PLoS One ;e The inflammatory response in myocardial injury, repair, and remodelling. Nat Rev Cardiol ;— Crossref PubMed Nian M, Lee P, Khaper N, et al. Inflammatory cytokines and postmyocardial infarction remodeling. Circ Res ;— Crossref PubMed Lv FH, Yin HL, He YQ, et al. Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF- κ B, PPAR- γ and Bcl-2 in rats with myocardial infarction injury. Exp Ther Med ;— Crossref PubMed Saeidinia A, Keihanian F, Butler AE, et al. Curcumin in heart failure: A choice for complementary therapy? Pharmacol Res ;—9. PubMed Wang NP, Pang XF. Zhang LH, et al. Attenuation of inflammatory response and reduction in infarct size by postconditioning are associated with downregulation of early growth response 1 during reperfusion in rat heart. Shock ;— Crossref PubMed Feldman AM, McNamara D. N Engl J Med ;— Crossref PubMed Fung G, Luo H, Qiu Y, et al. Crossref PubMed Fildes JE, Shaw SM, Yonan N, et al. The immune system and chronic heart failure: is the heart in control? Crossref PubMed Yndestad A, Damås JK, Øie E, et al. Role of inflammation in the progression of heart failure. Curr Cardiol Rep ;— Crossref PubMed Song Y, Ge W, Cai H, et al. J Cardiovasc Pharmacol Ther ;—9. Crossref PubMed Hernández M, Wicz S, Corral RS. Phytomedicine ;— Crossref PubMed Gao S, Zhou J, Liu N, et al. J Mol Cell Cardiol ;—9. Crossref PubMed Morimoto T, Sunagawa Y, Kawamura T, et al. The dietary compound curcumin inhibits p histone acetyltransferase activity and prevents heart failure in rats. Curcumin in heart failure: a choice for complementary therapy? Crossref PubMed Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD. Eur Respir J ;— Crossref PubMed Su B, Liu T, Fan H, et al. Inflammatory markers and the risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis. Crossref PubMed Sin DD, MacNee W. Am J Respir Crit Care Med ;—4. Crossref PubMed Moghaddam SJ, Barta P, Mirabolfathinejad SG, et al. Curcumin inhibits COPD-like airway inflammation and lung cancer progression in mice. Carcinogenesis ;— Crossref PubMed Yuan J, Liu R, Ma Y, et al. Curcumin attenuates airway inflammation and airway remolding by inhibiting NF- κ B signaling and COX-2 in cigarette smoke-induced COPD mice. Inflammation ;— Crossref PubMed Funamoto M, Sunagawa Y, Katanasaka Y, et al. Highly absorptive curcumin reduces serum atherosclerotic low-density lipoprotein levels in patients with mild COPD. Int J Chron Obstruct Pulmon Dis ;— Crossref PubMed Lee H, Lee IS, Choue R. Obesity, inflammation and diet. Pediatr Gastroenterol Hepatol Nutr ;— Crossref PubMed Schmidt FM, Weschenfelder J, Sander C, et al. Inflammatory cytokines in general and central obesity and modulating effects of physical activity. Crossref PubMed Kim SH, Després JP, Koh KK. Obesity and cardiovascular disease: friend or foe? Eur Heart J ;—8. Crossref PubMed Zhao Y, Chen B, Shen J, et al. The beneficial effects of quercetin, curcumin, and resveratrol in obesity. Oxid Med Cell Longev ; Crossref PubMed Pan Y, Zhao D, Yu N, et al. Curcumin improves glycolipid metabolism through regulating peroxisome proliferator activated receptor γ signalling pathway in high-fat diet-induced obese mice and 3T3-L1 adipocytes. R Soc Open Sci ; Crossref PubMed Ariamoghaddam AR, Ebrahimi-Hosseinzadeh B, Hatamian-Zarmi A, et al. In vivo anti-obesity efficacy of curcumin loaded nanofibers transdermal patches in high-fat diet induced obese rats. Mater Sci Eng C Mater Biol Appl ;— Crossref PubMed Jazayeri-Tehrani SA, Rezayat SM, Mansouri S, et al. Nano-curcumin improves glucose indices, lipids, inflammation, and Nesfatin in overweight and obese patients with non-alcoholic fatty liver disease NAFLD : a double-blind randomized placebo-controlled clinical trial. Nutr Metab Lond ; Crossref PubMed Chuengsamarn S, Rattanamongkolgul S, Phonrat B, et al. Reduction of atherogenic risk in patients with type 2 diabetes by curcuminoid extract: a randomized controlled trial. J Nutr Biochem ;— Crossref PubMed Panahi Y, Khalili N, Sahebi E, et al. Curcuminoids modify lipid profile in type 2 diabetes mellitus: a randomized controlled trial. Complement Ther Med ;—5. Crossref PubMed Darweesh SKL, Wolters FJ, Ikram MA, et al. Alzheimers Dement ;—9. Crossref PubMed Wyss-Coray T, Rogers J. Inflammation in Alzheimer disease — a brief review of the basic science and clinical literature. Cold Spring Harb Perspect Med ;2:a Crossref PubMed Justin BN, Turek M, Hakim AM. Heart disease as a risk factor for dementia. Clin Epidemiol ;— Crossref PubMed Seo EJ, Fischer N, Efferth T. Pharmacol Res ;— Crossref PubMed Liu ZJ, Li ZH, Liu L, et al. Front Pharmacol ; Crossref PubMed Small GW, Siddarth P, Li Z, et al. Memory and brain amyloid and tau effects of a bioavailable form of curcumin in non-demented adults: a double-blind, placebo-controlled month trial. Am J Geriatr Psychiatry ;— Crossref PubMed Adibian M, Hodaei H, Nikpayam O, et al. The effects of curcumin supplementation on high-sensitivity C-reactive protein, serum adiponectin, and lipid profile in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled trial. Phytother Res ;— Crossref PubMed Krishnareddy NT, Thomas JV, Nair S, et al. Biomed Res Int ; Crossref PubMed Mohammadi F, Ghazi-Moradi M, Ghayour-Mobarhan M, et al. The effects of curcumin on serum heat shock protein 27 antibody titers in patients with metabolic syndrome. J Diet Suppl — Crossref PubMed Vors C, Couillard C, Paradis ME, et al. Supplementation with resveratrol and curcumin does not affect the inflammatory response to a high-fat meal in older adults with abdominal obesity: a randomized, placebo-controlled crossover trial. J Nutr ;— Effects of curcuminoids plus piperine on glycemic, hepatic and inflammatory biomarkers in patients with type 2 diabetes mellitus: a randomized double-blind placebo-controlled trial. Drug Res Stuttg ;—9. Crossref PubMed Panahi Y, Alishiri GH, Parvin S, et al. Mitigation of systemic oxidative stress by curcuminoids in osteoarthritis: results of a randomized controlled trial. Risk of bias was assessed independently by 2 reviewers SQ and LFH using the Cochrane Handbook for Systematic Reviews of Interventions [ 30 ]. This tool allows for assessment of the study quality with respect to 6 domains: random sequence generation, allocation concealment, blinding, incomplete outcome data, selective reporting, and other bias. For each domain, the risk of bias was marked as low, unclear, or high. The meta-analysis was conducted by using Stata version In this analysis, only continuous variables were extracted. With use of relevant formulae [ 32 ], these values were also calculated from medians and ranges. Statistical heterogeneity between trials was detected by the Chi-squared and I -square I 2 tests. Subgroup analyses were conducted to explore heterogeneity among studies with respect to underlying disease and form of intervention turmeric or curcumin used. As only a single study had reported efficacy measures disaggregated by gender [ 27 ], subgroup analyses by gender could not be undertaken. Of the articles retrieved on initial literature search, a detailed evaluation of 11 full-text articles resulted in the elimination of 2 studies [ 33 , 34 ], due to the use of the same patient groups, and another 2 studies [ 35 , 36 ], owing to incomplete data Fig. Consequently, 7 randomized controlled trials RCTs , including a total of subjects, met the inclusion criteria and were selected for a qualitative analysis. Basic characteristics of the included RCTs are summarized in Table 1 , and the pre- and post-intervention serum lipid parameters are presented in Additional file 1 : Table S1. Of the 7 eligible studies, only studies that enrolled patients with T2DM [ 15 , 24 , 25 , 28 ] or MetS [ 23 , 26 , 27 ] were included. All studies were conducted in a double-blind manner with the exception of the trials by Selvi et al. Two of the studies were performed in Iran [ 23 , 24 ] and 2 [ 15 , 25 ] were conducted in India. The remaining studies were conducted in Pakistan [ 26 ], Taiwan [ 27 ], and Thailand [ 28 ], respectively. The duration of these studies ranged from 4 weeks to 6 months. Specified outcomes were reported from all studies, with the exception of the study by Chuengsamarn et al. The form of intervention and serum lipid parameters of studies at baseline and after intervention differed. The risk of bias in the individual studies is shown in Additional file 2 : Table S2. Overall, these selected studies varied in terms of quality: of the 7 RCTs, 4 were classified as high quality [ 24 , 26 , 27 , 28 ] and 3 were judged to be of moderate quality [ 15 , 23 , 25 ]. Four studies used appropriate randomization methods, such as a random number table [ 25 , 27 ] or a computer-generated list of random numbers [ 24 , 28 ]. Allocation concealment was only used in 4 studies [ 23 , 25 , 26 , 28 ]. Five trials used double-blinding of patients and practitioners [ 23 , 24 , 26 , 27 , 28 ]. All studies reported dropout rates and specific reasons for dropout with the exception of the trial by Chuengsamarn et al. Forest plot of the meta-analysis for comparison of plasma LDL-C concentrations between experimental and control groups. Forest plot of the meta-analysis for comparison of plasma HDL-C concentrations between experimental and control groups. Forest plot of the meta-analysis for comparison of plasma TG concentrations between experimental and control groups. Forest plot of the meta-analysis for comparison of plasma TC concentrations between experimental and control groups. To assess sources of potential bias, we conducted subgroup analyses by underlying diseases and forms of intervention—namely, studies in patients with hyperglycemia pre-diabetes and T2DM and MetS Table 2. Five RCTs reported adverse effects in both the control and experimental groups. Rahmani et al. Amin et al. Chuengsamarn et al. Moreover, 4 patients experienced side effects in the placebo group: vertigo and itching, constipation, and hot flashes in 1 patient each. Selvi et al. None of the remaining studies reported any adverse reactions of turmeric and curcumin therapy. No serious adverse reaction induced by turmeric and curcumin was reported in any of the studies included in this meta-analysis. The epidemic of obesity has contributed to a growing burden of CVD risk factors such as T2DM and MetS [ 37 ] defined as the presence of at least 3 out of the 4 criteria: central obesity, increased blood pressure, high blood sugar levels, and dyslipidemia [ 38 ]. Dyslipidemia is a well-established modifiable cardiovascular risk factor. All of the currently available antilipemic therapies have their own inherent shortcomings and disadvantages. Therefore, natural treatments have been investigated as potential therapies for lowering blood lipid levels. This systematic review of 7 randomized trials of turmeric and curcumin in patients at risk of CVD identified evidence of their beneficial effects on serum TG and LDL-C levels, although no significant difference was found with respect to serum HDL levels. When the analysis was restricted to more homogenous studies based on underlying disease in subjects hyperglycemia and MetS , a beneficial effect of turmeric and curcumin on serum TC levels was observed in subjects with MetS; however, in subjects with hyperglycemia, this beneficial effect on serum TC levels was not observed. It seems that the natural form turmeric and curcumin have more positive effects on patients suffering from MetS. With regard to the forms of intervention, turmeric extract may have a greater beneficial effect on serum TC levels, as compared to that of turmeric in its natural form. However, owing to the limited number of studies, definitive conclusions may not be drawn in this respect. Furthermore, larger scale trials are required among patients with MetS to explore the effect of turmeric extract, even in novel forms, in lowering plasma TC concentrations. Sahebkar conducted a meta-analysis of 5 RCTs to assess the effects of curcumin on blood lipid levels and found no significant improvements in the lipid profile in any aspect [ 22 ]. Several explanations could be tendered to explain why the results of their study were contrary to those of the present study. Firstly, both parallel and crossover randomized trials were selected, and these may have adversely influenced the final results. Secondly, most of the selected studies were conducted with unformulated curcumin, which is considered to have low bioavailability. Curcumin has poor bioavailability owing to its poor absorption, fast metabolism, and rapid elimination from the body. Some attempts have been made to overcome these deficits, including the use of a piperine black pepper adjuvant, liposomal curcumin, nanoparticles, phospholipid complexes, and an amorphous form [ 39 , 40 ]. Therefore, a hypothesis could be proposed that these novel dosage forms of curcumin may achieve greater clinical effects. To verify this theory, forest plots were conducted initially. Nevertheless, in our present review, only two trials [ 23 , 24 ] used novel forms, and the preparations used in these studies were dissimilar amorphous forms were used in one study [ 23 ] and nanoparticles were used in the other [ 24 ]. Therefore, further research on newer dosage forms of curcumin is required to confirm the hypothesis. Finally, differences with respect to underlying diseases in the study population may also explain this discrepancy. The authors included healthy participants and patients with various chronic diseases i. Even on performing a subgroup analysis in patients with high cardiovascular risk acute coronary syndrome, T2DM, or concomitant dyslipidemia and obesity , no significant difference could be identified because coronary artery disease is an end event rather than a risk factor for CVD. The article by Mohammadi et al. Unlike this study, in a trial among patients with coronary artery disease, although curcumin supplementation decreased serum levels of TC, LDL-C, and TG, there was no obvious difference when compared to placebo [ 41 ], possibly due to the small size of the study. Subsequently, a study by Soare et al. found that mg of curcumin did not influence plasma lipid levels in non-obese relatively healthy individuals [ 42 ]. Therefore, we tentatively propose that the antilipemic effect of curcumin is evident only in patients who are at a higher risk of cardiovascular morbidity, such as those with MetS, T2DM, and obesity. Some molecular mechanisms could potentially explain these results. Insulin resistance IR is the basic underlying pathology in both T2DM and MetS. Neerati et al. reported that curcumin could counter IR [ 43 ]. Through amelioration of metabolic derangement and potential binding of curcumin with peroxisome proliferator-activated receptor gamma PPAR-γ as agonist, curcumin could play a preventive role in diet-induced insulin resistance [ 44 ]. Moreover, curcumin was shown to increase activation of PPAR-γ [ 45 ], which suppressed expression of the LDL-C receptor gene, and could thereby reduce plasma LDL-C concentrations [ 46 ]. Because it interacts with multiple targets, including peroxisome proliferator-activated receptor alpha PPAR-α , PPAR-γ, cholesteryl ester transfer protein CETP , and lipoprotein lipase, curcumin could probably play a role in reduction of triglyceride levels [ 47 , 48 , 49 ]. Furthermore, curcumin is expected to affect both synthesis and catabolism of triglyceride-rich lipoproteins [ 47 , 48 , 49 ]. Thus, curcumin supplementation may lower plasma triglycerides and cholesterol concentrations by mitigating the expressions of lipogenic genes [ 48 , 49 , 50 ]. Additionally, the lipid-lowering effect of turmeric and curcumin is related to statins. Panahi et al. found that curcumin affected all pathways of cholesterol metabolism that are affected by statin therapy; it also reduced the effective doses of statins, which helped reduce the incidence of serious adverse reactions [ 51 ]. Furthermore, curcumin might serve as a valuable adjunct to statin therapy in patients with disordered lipid metabolism [ 51 ]. In our meta-analysis, we found that consumption of turmeric and curcumin was safe and well-tolerated in general. Several potential limitations of this review need mention. First, the most important limitation may pertain to the interpretability of outcomes. Third, all subjects in the included studies were Asians. Lastly, some data were obtained indirectly, and those could have affected the accuracy of both the overall effects and the results of subgroup analyses. Subjects who received turmeric and curcumin experienced a natural cardioprotective effect, with lowering of serum LDL-C and TG levels, as compared to subjects who did not. The efficacy of turmeric and curcumin on serum TC levels remains inconclusive, despite their superior efficacy observed in patients with MetS. A greater effect of turmeric extract in reducing serum TC levels may be observed in patients who are at risk of CVD; however, this finding needs to be confirmed in future studies. No significant change in serum HDL levels was observed. Due to uncertainties related to dosage form, dose and medication frequency, it is premature to recommend the use of turmeric or curcumin in clinical settings. Nonetheless, the analysis does provide a synthesis of the currently available evidence and supports larger scale clinical trials of curcumin. World Health Organization: The Top 10 Causes of Death. html Accessed 20 Nov Srikanth S, Deedwania P. Management of Dyslipidemia in patients with hypertension, diabetes, and metabolic syndrome. Curr Hypertens Rep. Article PubMed Google Scholar. Musunuru K. Atherogenic dyslipidemia: cardiovascular risk and dietary intervention. Article CAS PubMed PubMed Central Google Scholar. Padala S, Thompson PD. Statins as a possible cause of inflammatory and necrotizing myopathies. Article CAS PubMed Google Scholar. Chalasani N. Statins and hepatotoxicity: focus on patients with fatty liver. Sniderman AD. Is there value in liver function test and creatine phosphokinase monitoring with statin use? Am J Cardiol. Law M, Rudnicka AR. Statin safety: a systematic review. Goel A, Kunnumakkara AB, Aggarwal BB. Biochem Pharmacol. Sahebkar A. Why it is necessary to translate curcumin into clinical practice for the prevention and treatment of metabolic syndrome? Kunnumakkara AB, Bordoloi D, Padmavathi G, Monisha J, Roy NK, Prasad S, Aggarwal BB. Curcumin, the golden nutraceutical: multitargeting for multiple chronic diseases. Br J Pharmacol. Pulido-Moran M, Moreno-Fernandez J, Ramirez-Tortosa C, Ramirez-Tortosa M. Curcumin and health. Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Sripradha R, Badhe B. Curcumin inhibits hyperlipidemia and hepatic fat accumulation in high-fructose-fed male Wistar rats. Pharm Biol. Li ZY, Ding LL, Li JM, Xu BL, Yang L, Bi KS, Wang ZT. PLoS One. Article PubMed PubMed Central Google Scholar. Shin SK, Ha TY, McGregor RA, Choi MS. Long-term curcumin administration protects against atherosclerosis via hepatic regulation of lipoprotein cholesterol metabolism. Mol Nutr Food Res. Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N. Effect of NCB, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study. Drugs R D. But a double-blind, placebo-controlled study found that taking curcumin, the active ingredient in turmeric, at a dose of up to 4 g per day did not improve cholesterol levels. There has been a great deal of research on turmeric's anti-cancer properties, but results are still preliminary. Evidence from test tube and animal studies suggests that curcumin may help prevent or treat several types of cancers, including prostate, breast, skin, and colon cancer. Tumeric's preventive effects may relate to its antioxidant properties, which protect cells from damage. More research is needed. Cancer should be treated with conventional medications. Don't use alternative therapies alone to treat cancer. If you choose to use complementary therapies along with your cancer treatment, make sure you tell all your doctors. Test tube and animal studies suggest turmeric may kill bacteria and viruses, but researchers don't know whether it would work in people. A preliminary study suggests curcumin may help treat uveitis, an inflammation of the eye's iris. Preliminary research suggests that curcumin may be as effective as corticosteroids, the type of medication usually prescribed. Tumeric's powerful antioxidant, anti-inflammatory, and circulatory effects may help prevent and treat neurodegenerative diseases, including Alzheimer disease, Parkinson's disease, multiple sclerosis, and other conditions. A relative of ginger, turmeric is a perennial plant that grows 5 to 6 feet high in the tropical regions of Southern Asia, with trumpet-shaped, dull yellow flowers. Its roots are bulbs that also produce rhizomes, which then produce stems and roots for new plants. Turmeric is fragrant and has a bitter, somewhat sharp taste. Although it grows in many tropical locations, the majority of turmeric is grown in India, where it is used as a main ingredient in curry. The roots, or rhizomes and bulbs, are used in medicine and food. They are generally boiled and then dried, turning into the familiar yellow powder. Curcumin, the active ingredient, has antioxidant properties. Other substances in this herb have antioxidant properties as well. Bromelain increases the absorption and anti-inflammatory effects of curcumin, so it is often combined with turmeric products. Pediatric Turmeric supplements haven't been studied in children, so there is no recommended dose. The use of herbs is a time-honored approach to strengthening the body and treating disease. However, herbs can trigger side effects and may interact with other herbs, supplements, or medications. For these reasons, you should take herbs with care, under the supervision of a health care provider. Turmeric in food is considered safe. However, taking large amounts of turmeric and curcumin in supplement form for long periods of time may cause stomach upset and, in extreme cases, ulcers. People who have gallstones or obstruction of the bile passages should talk to their doctor before taking turmeric. If you have diabetes, talk to your doctor before taking turmeric supplements. Turmeric may lower blood sugar levels. When combined with medications for diabetes, turmeric could cause hypoglycemia low blood sugar. Although it is safe to eat foods with turmeric, pregnant and breastfeeding women should not take turmeric supplements. Because turmeric may act like a blood thinner, you should stop taking it at least 2 weeks before surgery. Tell your doctor and surgeon that you have been taking turmeric. If you are being treated with any of the following medications, you should not use turmeric or curcumin in medicinal forms without first talking to your health care provider. Turmeric may strengthen the effects of these drugs, raising the risk of bleeding. Blood thinners include warfarin Coumadin , clopidogrel Plavix , and aspirin, among others. Turmeric may interfere with the action of these drugs, increasing the production of stomach acid:. Turmeric may strengthen the effects of these drugs, increasing the risk of hypoglycemia low blood sugar. Aggarwal BB, Yuan W, Li S, Gupta SC. Curcumin-free tumeric exhibits anti-inflammatory and anticancer activities: Identification of novel components of tumeric. Mol Nutr Food Res. Aggarwal BB, Sundaram C, Malani N, Ichikawa H. Curcumin: the Indian solid gold. Adv Exp Med Biol. Asai A, Miyazawa T. Dietary curcuminoids prevent high-fat diet-induced lipid accumulation in rat liver and epididymal adipose tissue. J Nutr. Asher GN, Spelman K. Clinical utility of curcumin extract. Altern Ther Health Med. Baum L, Cheung SK, Mok VC, et al. Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol Res. Blumenthal M, Goldberg A, Brinckmann J. Herbal Medicine: Expanded Commission E Monographs. Newton, MA: Integrative Medicine Communications; Bolognia JL, Jorizzo JL, Schaffer JV, eds. Philadelphia, PA: Elsevier Saunders; Darvesh AS, Aggarwal BB, Bishayee A. Curcumin and Liver Cancer: A Review. Curr Pharm Biotechnol. Davis JM, Murphy EA, Carmichael MD, et al. Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage. Am J Physiol Regul Integr Comp Physiol. |
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| Plant Description | Disclosure: The authors have no conflicts of interest to declare. View author publications. Specifically, the lower limit of the one-sided confidence interval CI; confidence coefficient: 0. conducted a clinical trial including patients with mild COPD in which the oxidised LDL — alphaantitrypsin LDL — was significantly decreased in those taking highly absorbable curcumin compared with those taking a placebo. sustained ventricular tachycardia and ventricular fibrillation or bradycardia indicated for an implanted pacemaker and those with an implanted pacemaker. A animal study also found that curcumin may help reduce anxiety, though studies on humans are needed to verify this. |
Curcumin and Heart Disease -
Two independent investigators SQ and LFH screened the titles and abstracts of articles initially retrieved on online search of databases, and extracted essential data from eligible full-text articles.
Data on study design, patient characteristics, number of patients, treatment regimen, duration of treatment, year of publication, and daily dose of curcumin or turmeric powder were extracted, as were the mean ± SD or mean ± SE of all efficacy measures specified earlier.
To control relative heterogeneity, only data of efficacy measures pertaining to the study period between 4 weeks and 3 months were extracted.
For studies with missing data, authors were sent emails requesting details of these data. Risk of bias was assessed independently by 2 reviewers SQ and LFH using the Cochrane Handbook for Systematic Reviews of Interventions [ 30 ].
This tool allows for assessment of the study quality with respect to 6 domains: random sequence generation, allocation concealment, blinding, incomplete outcome data, selective reporting, and other bias. For each domain, the risk of bias was marked as low, unclear, or high.
The meta-analysis was conducted by using Stata version In this analysis, only continuous variables were extracted. With use of relevant formulae [ 32 ], these values were also calculated from medians and ranges. Statistical heterogeneity between trials was detected by the Chi-squared and I -square I 2 tests.
Subgroup analyses were conducted to explore heterogeneity among studies with respect to underlying disease and form of intervention turmeric or curcumin used. As only a single study had reported efficacy measures disaggregated by gender [ 27 ], subgroup analyses by gender could not be undertaken.
Of the articles retrieved on initial literature search, a detailed evaluation of 11 full-text articles resulted in the elimination of 2 studies [ 33 , 34 ], due to the use of the same patient groups, and another 2 studies [ 35 , 36 ], owing to incomplete data Fig.
Consequently, 7 randomized controlled trials RCTs , including a total of subjects, met the inclusion criteria and were selected for a qualitative analysis.
Basic characteristics of the included RCTs are summarized in Table 1 , and the pre- and post-intervention serum lipid parameters are presented in Additional file 1 : Table S1. Of the 7 eligible studies, only studies that enrolled patients with T2DM [ 15 , 24 , 25 , 28 ] or MetS [ 23 , 26 , 27 ] were included.
All studies were conducted in a double-blind manner with the exception of the trials by Selvi et al. Two of the studies were performed in Iran [ 23 , 24 ] and 2 [ 15 , 25 ] were conducted in India. The remaining studies were conducted in Pakistan [ 26 ], Taiwan [ 27 ], and Thailand [ 28 ], respectively.
The duration of these studies ranged from 4 weeks to 6 months. Specified outcomes were reported from all studies, with the exception of the study by Chuengsamarn et al.
The form of intervention and serum lipid parameters of studies at baseline and after intervention differed.
The risk of bias in the individual studies is shown in Additional file 2 : Table S2. Overall, these selected studies varied in terms of quality: of the 7 RCTs, 4 were classified as high quality [ 24 , 26 , 27 , 28 ] and 3 were judged to be of moderate quality [ 15 , 23 , 25 ].
Four studies used appropriate randomization methods, such as a random number table [ 25 , 27 ] or a computer-generated list of random numbers [ 24 , 28 ]. Allocation concealment was only used in 4 studies [ 23 , 25 , 26 , 28 ].
Five trials used double-blinding of patients and practitioners [ 23 , 24 , 26 , 27 , 28 ]. All studies reported dropout rates and specific reasons for dropout with the exception of the trial by Chuengsamarn et al.
Forest plot of the meta-analysis for comparison of plasma LDL-C concentrations between experimental and control groups. Forest plot of the meta-analysis for comparison of plasma HDL-C concentrations between experimental and control groups. Forest plot of the meta-analysis for comparison of plasma TG concentrations between experimental and control groups.
Forest plot of the meta-analysis for comparison of plasma TC concentrations between experimental and control groups. To assess sources of potential bias, we conducted subgroup analyses by underlying diseases and forms of intervention—namely, studies in patients with hyperglycemia pre-diabetes and T2DM and MetS Table 2.
Five RCTs reported adverse effects in both the control and experimental groups. Rahmani et al. Amin et al. Chuengsamarn et al. Moreover, 4 patients experienced side effects in the placebo group: vertigo and itching, constipation, and hot flashes in 1 patient each.
Selvi et al. None of the remaining studies reported any adverse reactions of turmeric and curcumin therapy. No serious adverse reaction induced by turmeric and curcumin was reported in any of the studies included in this meta-analysis. The epidemic of obesity has contributed to a growing burden of CVD risk factors such as T2DM and MetS [ 37 ] defined as the presence of at least 3 out of the 4 criteria: central obesity, increased blood pressure, high blood sugar levels, and dyslipidemia [ 38 ].
Dyslipidemia is a well-established modifiable cardiovascular risk factor. All of the currently available antilipemic therapies have their own inherent shortcomings and disadvantages.
Therefore, natural treatments have been investigated as potential therapies for lowering blood lipid levels. This systematic review of 7 randomized trials of turmeric and curcumin in patients at risk of CVD identified evidence of their beneficial effects on serum TG and LDL-C levels, although no significant difference was found with respect to serum HDL levels.
When the analysis was restricted to more homogenous studies based on underlying disease in subjects hyperglycemia and MetS , a beneficial effect of turmeric and curcumin on serum TC levels was observed in subjects with MetS; however, in subjects with hyperglycemia, this beneficial effect on serum TC levels was not observed.
It seems that the natural form turmeric and curcumin have more positive effects on patients suffering from MetS. With regard to the forms of intervention, turmeric extract may have a greater beneficial effect on serum TC levels, as compared to that of turmeric in its natural form.
However, owing to the limited number of studies, definitive conclusions may not be drawn in this respect. Furthermore, larger scale trials are required among patients with MetS to explore the effect of turmeric extract, even in novel forms, in lowering plasma TC concentrations.
Sahebkar conducted a meta-analysis of 5 RCTs to assess the effects of curcumin on blood lipid levels and found no significant improvements in the lipid profile in any aspect [ 22 ]. Several explanations could be tendered to explain why the results of their study were contrary to those of the present study.
Firstly, both parallel and crossover randomized trials were selected, and these may have adversely influenced the final results.
Secondly, most of the selected studies were conducted with unformulated curcumin, which is considered to have low bioavailability. Curcumin has poor bioavailability owing to its poor absorption, fast metabolism, and rapid elimination from the body.
Some attempts have been made to overcome these deficits, including the use of a piperine black pepper adjuvant, liposomal curcumin, nanoparticles, phospholipid complexes, and an amorphous form [ 39 , 40 ]. Therefore, a hypothesis could be proposed that these novel dosage forms of curcumin may achieve greater clinical effects.
To verify this theory, forest plots were conducted initially. Nevertheless, in our present review, only two trials [ 23 , 24 ] used novel forms, and the preparations used in these studies were dissimilar amorphous forms were used in one study [ 23 ] and nanoparticles were used in the other [ 24 ].
Therefore, further research on newer dosage forms of curcumin is required to confirm the hypothesis. Finally, differences with respect to underlying diseases in the study population may also explain this discrepancy.
The authors included healthy participants and patients with various chronic diseases i. Even on performing a subgroup analysis in patients with high cardiovascular risk acute coronary syndrome, T2DM, or concomitant dyslipidemia and obesity , no significant difference could be identified because coronary artery disease is an end event rather than a risk factor for CVD.
The article by Mohammadi et al. Unlike this study, in a trial among patients with coronary artery disease, although curcumin supplementation decreased serum levels of TC, LDL-C, and TG, there was no obvious difference when compared to placebo [ 41 ], possibly due to the small size of the study.
Subsequently, a study by Soare et al. found that mg of curcumin did not influence plasma lipid levels in non-obese relatively healthy individuals [ 42 ].
Therefore, we tentatively propose that the antilipemic effect of curcumin is evident only in patients who are at a higher risk of cardiovascular morbidity, such as those with MetS, T2DM, and obesity. Some molecular mechanisms could potentially explain these results. Insulin resistance IR is the basic underlying pathology in both T2DM and MetS.
Neerati et al. reported that curcumin could counter IR [ 43 ]. Through amelioration of metabolic derangement and potential binding of curcumin with peroxisome proliferator-activated receptor gamma PPAR-γ as agonist, curcumin could play a preventive role in diet-induced insulin resistance [ 44 ].
Moreover, curcumin was shown to increase activation of PPAR-γ [ 45 ], which suppressed expression of the LDL-C receptor gene, and could thereby reduce plasma LDL-C concentrations [ 46 ].
Because it interacts with multiple targets, including peroxisome proliferator-activated receptor alpha PPAR-α , PPAR-γ, cholesteryl ester transfer protein CETP , and lipoprotein lipase, curcumin could probably play a role in reduction of triglyceride levels [ 47 , 48 , 49 ].
Furthermore, curcumin is expected to affect both synthesis and catabolism of triglyceride-rich lipoproteins [ 47 , 48 , 49 ]. Thus, curcumin supplementation may lower plasma triglycerides and cholesterol concentrations by mitigating the expressions of lipogenic genes [ 48 , 49 , 50 ].
Additionally, the lipid-lowering effect of turmeric and curcumin is related to statins. Panahi et al. found that curcumin affected all pathways of cholesterol metabolism that are affected by statin therapy; it also reduced the effective doses of statins, which helped reduce the incidence of serious adverse reactions [ 51 ].
Furthermore, curcumin might serve as a valuable adjunct to statin therapy in patients with disordered lipid metabolism [ 51 ]. In our meta-analysis, we found that consumption of turmeric and curcumin was safe and well-tolerated in general. Several potential limitations of this review need mention.
First, the most important limitation may pertain to the interpretability of outcomes. Third, all subjects in the included studies were Asians.
Lastly, some data were obtained indirectly, and those could have affected the accuracy of both the overall effects and the results of subgroup analyses. Subjects who received turmeric and curcumin experienced a natural cardioprotective effect, with lowering of serum LDL-C and TG levels, as compared to subjects who did not.
The efficacy of turmeric and curcumin on serum TC levels remains inconclusive, despite their superior efficacy observed in patients with MetS.
A greater effect of turmeric extract in reducing serum TC levels may be observed in patients who are at risk of CVD; however, this finding needs to be confirmed in future studies.
No significant change in serum HDL levels was observed. Due to uncertainties related to dosage form, dose and medication frequency, it is premature to recommend the use of turmeric or curcumin in clinical settings.
Nonetheless, the analysis does provide a synthesis of the currently available evidence and supports larger scale clinical trials of curcumin. World Health Organization: The Top 10 Causes of Death. html Accessed 20 Nov Srikanth S, Deedwania P.
Management of Dyslipidemia in patients with hypertension, diabetes, and metabolic syndrome. Curr Hypertens Rep. Article PubMed Google Scholar. Musunuru K. Atherogenic dyslipidemia: cardiovascular risk and dietary intervention. Article CAS PubMed PubMed Central Google Scholar.
Padala S, Thompson PD. Statins as a possible cause of inflammatory and necrotizing myopathies. Article CAS PubMed Google Scholar. Chalasani N. Statins and hepatotoxicity: focus on patients with fatty liver. Sniderman AD. Is there value in liver function test and creatine phosphokinase monitoring with statin use?
Am J Cardiol. Law M, Rudnicka AR. Statin safety: a systematic review. Goel A, Kunnumakkara AB, Aggarwal BB. Biochem Pharmacol. Sahebkar A. Why it is necessary to translate curcumin into clinical practice for the prevention and treatment of metabolic syndrome?
Kunnumakkara AB, Bordoloi D, Padmavathi G, Monisha J, Roy NK, Prasad S, Aggarwal BB. Curcumin, the golden nutraceutical: multitargeting for multiple chronic diseases.
Br J Pharmacol. Pulido-Moran M, Moreno-Fernandez J, Ramirez-Tortosa C, Ramirez-Tortosa M. Curcumin and health. Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Sripradha R, Badhe B. Curcumin inhibits hyperlipidemia and hepatic fat accumulation in high-fructose-fed male Wistar rats. Pharm Biol.
Li ZY, Ding LL, Li JM, Xu BL, Yang L, Bi KS, Wang ZT. PLoS One. Article PubMed PubMed Central Google Scholar. Shin SK, Ha TY, McGregor RA, Choi MS. Long-term curcumin administration protects against atherosclerosis via hepatic regulation of lipoprotein cholesterol metabolism.
Mol Nutr Food Res. Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N. Effect of NCB, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study.
Drugs R D. Soni KB, Kuttan R. Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian J Physiol Pharmacol. CAS PubMed Google Scholar. Ramirez-Bosca A, Soler A, Carrion MA, Diaz-Alperi J, Bernd A, Quintanilla C, Quintanilla Almagro E, Miquel J.
Implications for atherogenesis prevention. Mech Ageing Dev. Pungcharoenkul K, Thongnopnua P. Effect of different curcuminoid supplement dosages on total in vivo antioxidant capacity and cholesterol levels of healthy human subjects.
Phytother Res. Mohammadi A, Sahebkar A, Iranshahi M, Amini M, Khojasteh R, Ghayour-Mobarhan M, Ferns GA. Effects of supplementation with curcuminoids on dyslipidemia in obese patients: a randomized crossover trial. Baum L, Cheung SK, Mok VC, Lam LC, Leung VP, Hui E, Ng CC, Chow M, Ho PC, Lam S, et al.
Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol Res. Alwi I, Santoso T, Suyono S, Sutrisna B, Suyatna FD, Kresno SB, Ernie S. The effect of curcumin on lipid level in patients with acute coronary syndrome. Acta Med Indones.
PubMed Google Scholar. A systematic review and meta-analysis of randomized controlled trials investigating the effects of curcumin on blood lipid levels. Clin Nutr. Rahmani S, Asgary S, Askari G, Keshvari M, Hatamipour M, Feizi A, Sahebkar A.
Treatment of non-alcoholic fatty liver disease with Curcumin: a randomized placebo-controlled trial. Rahimi HR, Mohammadpour AH, Dastani M, Jaafari MR, Abnous K, Ghayour Mobarhan M, Kazemi OR. The effect of nano-curcumin on HbA1c, fasting blood glucose, and lipid profile in diabetic subjects: a randomized clinical trial.
Avicenna J Phytomed. PubMed PubMed Central Google Scholar. Maithili Karpaga Selvi N, Sridhar MG, Swaminathan RP, Sripradha R. Efficacy of turmeric as adjuvant therapy in type 2 diabetic patients. Indian J Clin Biochem. Amin F, Islam N, Anila N, Gilani AH.
Clinical efficacy of the co-administration of turmeric and black seeds Kalongi in metabolic syndrome - a double blind randomized controlled trial - TAK-MetS trial. Complement Ther Med. Yang YS, Su YF, Yang HW, Lee YH, Chou JI, Ueng KC. Lipid-lowering effects of curcumin in patients with metabolic syndrome: a randomized, double-blind, placebo-controlled trial.
Chuengsamarn S, Rattanamongkolgul S, Phonrat B, Tungtrongchitr R, Jirawatnotai S. Reduction of atherogenic risk in patients with type 2 diabetes by curcuminoid extract: a randomized controlled trial.
J Nutr Biochem. Daily JW, Yang M, Park S. Efficacy of turmeric extracts and Curcumin for alleviating the symptoms of joint arthritis: a systematic review and meta-analysis of randomized clinical trials. J Med Food. Higgins JP, Altman DG, Gotzsche PC, Juni P, Moher D, Oxman AD, Savovic J, Schulz KF, Weeks L, Sterne JA, et al.
The Cochrane Collaboration's tool for assessing risk of bias in randomised trials. Higgins JPT, Green S, editors. Cochrane handbook for systematic reviews of interventions version 5.
The Cochrane Collaboration; Hozo SP, Djulbegovic B, Hozo I. Estimating the mean and variance from the median, range, and the size of a sample. BMC Med Res Methodol. Panahi Y, Khalili N, Hosseini MS, Abbasinazari M, Sahebkar A. Lipid-modifying effects of adjunctive therapy with curcuminoids-piperine combination in patients with metabolic syndrome: results of a randomized controlled trial.
Sahebkar A, Mohammadi A, Atabati A, Rahiman S, Tavallaie S, Iranshahi M, Akhlaghi S, Ferns GA, Ghayour-Mobarhan M.
Curcuminoids modulate pro-oxidant-antioxidant balance but not the immune response to heat shock protein 27 and oxidized LDL in obese individuals. Panahi Y, Hosseini MS, Khalili N, Naimi E, Soflaei SS, Majeed M, Sahebkar A. Effects of supplementation with curcumin on serum adipokine concentrations: a randomized controlled trial.
Panahi Y, Hosseini MS, Khalili N, Naimi E, Simental-Mendia LE, Majeed M, Sahebkar A. Effects of curcumin on serum cytokine concentrations in subjects with metabolic syndrome: a post-hoc analysis of a randomized controlled trial.
Biomed Pharmacother. Heinl RE, Dhindsa DS, Mahlof EN, Schultz WM, Ricketts JC, Varghese T, Esmaeeli A, Allard-Ratick MP, Millard AJ, Kelli HM, et al. Comprehensive cardiovascular risk reduction and cardiac rehabilitation in diabetes and the metabolic syndrome.
Can J Cardiol. Brede S, Serfling G, Klement J, Schmid SM, Lehnert H. EDA-Fibronectin , Periostin , Vimentin , α-SMA , p -SMAD3 , CD68 , CD3 and Troponin I were purchased from Abcam, Inc.
ECL western blot detection kits FD were purchased from FD bio Science Biological Technology Co. A cell counting kit-8 CCK-8 dye was purchased from Biosharp, Inc. Isoflurane was obtained from RWD Life Science Co. Picro Sirius Red BP-DL was obtained from Sbjbio Nanjing SenBeiJia Biological Technology Co.
ELISA kit was used to quantify IL ml Shanghai Enzyme-linked Biotechnology Co. All experiments were approved by the Ethical Committee of Zhejiang University and all surgical procedures were performed by experienced technician sin a blinded manner.
Mice were acclimatized to the standard conditions with 12 h lighting cycle, 25 ± 2°C temperature, free access to water and standard chow for 1 week. Then, they were sorted into four groups of 10 mice per group.
Group 1 sham received dimethylsulfoxide DMSO-saline for 28 days intragastrically i. as a vehicle for curcumin. for 28 days after MI. MI was induced by ligation of the left anterior descending coronary artery. The MI model was established as described previously Hu et al. During 4 weeks treatment, mice was anaesthetized 1.
Two-dimensional B-mode and M-mode measurements in the long-axis view level include left ventricular end-diastolic dimension LVID,d , left ventricular end-systolic dimension LVID,s , interventricular septal wall thickness in diastole IVS,d and in systole IVS,s , and left ventricular posterior wall thickness in diastole LVPW,d and in systole LVPW,s.
Left ventricular ejection fraction and fractional shortening were automatically calculated by the echocardiographic system Xiao et al. The sections were then stained with a In Situ Cell Death Detection Kit Roche Applied Science, CH , CD3, CD68, Troponin I Abcam, United Kingdom , and DAPI Vector Laboratories, Burlingame, CA, United States.
After deparaffinization, sections were stained with Sirius Red. Tissue damage was scored by calculating the scar circumference, including both internal and external scar diameters. The sirius red—stained sections were scanned with a microscope digital camera Olympus Instrument, United States , and Biotechnologies, China.
The percentage of fibrotic area was calculated as the mean value of the endocardial and epicardial length of the whole fibrotic area in proportion to the mean length of the endocardial and epicardial left ventricle using Image using Image Pro Plus software version 6.
Mouse macrophage-like Raw After 2 days, the medium was replaced, and nonadherent cells were discarded. Following treatment, 10 μL of CCK-8 solution was added to each well and incubated for 2 h. The absorbance of each well was measured at and nm using a microplate reader Spark TECAN, Switzerland.
All data were calculated from triplicate samples. Cell apoptosis was evaluated by flow cytometry with Annexin V-FITC and PI staining CytoFlex, Beckman Coulter, Germany. NRCFs in each group were seeded in a 6-well plate at 2 × 10 5 cells per well and cultured in FBS free medium overnight.
NRCFs were transfected for 48 h with 2 μg of the IL18 mimic IL rat, Shanghai GenePharma Co. Real-time fluorescent quantitative polymerase chain reaction RT-qPCR and enzyme-linked immunosorbent assay ELISA were used to quantify IL transfection efficiency.
And resultant cDNA samples were subjected to qPCR on LightCycler ® PCR System Roche using SYBR ® Green Premix Pro Taq HS qPCR Kit AG. The upstream and downstream primers of IL6, IL-1β, and TNF-α were designed and synthesized by Tsingke Biotechnology Co.
The primer sequences used were as follows:. The cells seeded in the 6-well plates were collected, lysed in 2. Finally, the immunoreactive protein was detected by a chemiluminescence assay AIRGB, GE HealthCare, United States using the FDbio-Dura ECL kit FDbio Science Biological Technology Co.
All results were expressed as value ±standard error of the mean SEM. Statistical calculations were carried out using GraphPad Prism 9. To test the effect of curcumin on MI, we performed MI surgery by permanent ligation of the left anterior descending artery followed by intragastric administration of curcumin for 7 days or 28 days.
In parallel, a placebo post-MI group was also established. To summarize, the administration of curcumin after MI significantly ameliorated inflammation in the acute phase; however, curcumin exerted a protective effect by preserving long-term cardiac function only after MI, which suggested that the reduced inflammation activation might be related to adverse cardiac remodeling mediated by curcumin intake.
FIGURE 1. Curcumin administration ameliorates inflammatory response in acute phase post-MI and preserves long-term cardiac function A.
Troponins were identified by green coloring; statistical data are summarized in B. Troponins were identified by green coloring; statistical data are summarized in D. Echocardiography were conducted at baseline and 3, 7, 14, and 28 days post-MI. Left ventricular internal dimension in systolic phase LVID s and Left ventricular internal dimension in diastolic phase LVID d in each group at different timepoint were also plotted in H and I.
MI: myocardial infarction. Results are mean with SEM. As previously indicated, curcumin delivery significantly improved long-term cardiac function after MI in C57 mice. To determine what yields this beneficial effect, we conducted TUNEL and picro sirius red staining and, surprisingly, discovered no significant reduction in anti-apoptotic effect on cardiomyocyte within border area in the curcumin-treated group compared with the placebo group 7 days after MI Supplementary Figure S1A,B.
However, we observed dramatically reduced scar formation reflected by picro sirius red staining in both scar circumference and infarct size dimension in curcumin group compared with the placebo group Figures 2A—C. The results presented above indicate that the use of curcumin following MI significantly improved cardiac function by inhibiting excessive collagen deposition and scar formation.
FIGURE 2. Curcumin reduces scar formation and ameliorates adverse cardiac remodeling in post-MI rats in long-term prospects A-B. Representative images of sirius red staining of whole heart cross section in rat heart from all groups, as indicated A B Statistical analysis of scar circumference in each group means with SEM.
Collagen summary and statistics are plotted in E F-G. It is known that LPS significantly activate inflammation and mobilize macrophage proliferation as well as M1 polarization. To further investigate the mechanism of curcumin in anti-inflammatory processes, we performed LPS stimulation on macrophage in vitro for 24 h followed by Curcumin administration, CCK8 test revealed dramatic inhibited macrophage proliferation when dosage was 20 uM, indicating Curcumin might exerted anti-proliferation or pro-apoptotic effect in macrophages under LPS stimulation Figure 3A.
Flow cytometry was conducted to determine whether curcumin promoted macrophage apoptosis under LPS stimulation. As shown in Figures 3B,C , curcumin significantly increased macrophage apoptosis under LPS stimulation compared with LPS only also using 20 uM dosage.
In addition, the cleaved-caspase three protein level, which acts as a marker of apoptosis, was also significantly up-regulated in the curcumin-treated macrophages with LPS group compared with LPS only reflected by western blot Figures 3D,E.
Furthermore, macrophage activation could induce the secretion of pro-inflammatory cytokines such as IL-6, IL1β, and TNF-α to initiate an immune response to ischemic injury, thus aggravating cardiomyocyte apoptosis; however, curcumin treatment significantly inhibited pro-inflammatory cytokine secretion in macrophages with LPS group compared with LPS only, as reflected by reduced IL-6, IL-1β, and TNF-α secretion especially at 20 uM concentration Figures 3F—H.
These data indicate that the administration of curcumin on macrophages under LPS stimulation exerted both pro-apoptotic effects in macrophages and anti-inflammatory effects by reducing cytokine release from macrophages, which could be greatly beneficial post-MI. FIGURE 3.
Curcumin promotes macrophage apoptosis in vitro and restrain pro-inflammatory cytokine secretio A. As previously mentioned, curcumin has also been shown to regulate macrophage polarization by increasing anti-inflammatory cytokine IL levels and decreasing the M1 phenotype marker CD86 along with the pro-inflammatory cytokines TNF-α and IL To validate whether curcumin exerted an inhibitory effect on cardiac fibrosis by alleviating inflammation-induced fibrosis or by directly suppressing cardiac fibroblast trans -differentiation and collagen secretion, we co-cultured macrophages under LPS stimulation with isolated primary neonatal rat cardiac fibroblasts in vitro followed by TGF-β stimulation in NRCF for 24 h, Surprisingly, we discovered that curcumin administration in macrophages with LPS stimulation significantly mitigated collagen synthesis from co-cultured NRCF, which was revealed by pro-fibrotic protein expression α-SMA, Vimentin, Periostin, and EDA-Fibronectin Figure 4A,C—F.
In contrast, we did not observe a significant change in fibrosis protein expression when curcumin was directly added to NRCF treated with TGF-β for 24 h compared with the TGF-β only group Figure 4B,G—J. FIGURE 4. Curcumin inhibits cardiac fibrosis by regulating macrophage-fibroblast crosstalk instead of directly suppressing cardiac fibroblast trans -differentiation A.
Summary data of protein expression are displayed in A , EDA-fibronectin are plotted in C , periostin is plotted in D , vimentin is plotted in E and α-SMA is plotted in F G — J. Summary data of protein expression displayed in B , EDA-Fibronectin was plotted in G , periostin was plotted in H , vimentin is plotted in I and α-SMA in J K — M.
To elucidate the detailed mechanism of the identified curcumin-mediated anti-fibrosis effect, we performed bulk mRNA sequencing in NRCF co-cultured with curcumin-treated macrophages and NRCF co-cultured with PBS-treated macrophages; genes were downregulated and 1, genes were upregulated in the curcumin group compared with the PBS group Figures 5A,B.
Gene enrichment from GO pathway analysis revealed that both immune and defense response signaling were mostly activated and altered between the two groups and that these two signaling pathways were classified and regulated by defense response regulation, indicating the pivotal utilization of curcumin in alleviating an overreactive immune response Figures 5C,D , the top 10 up-regulated and down-regulated genes enriched in immune response signaling are listed in Table 1.
Among all altered genes enriched in immune response signaling, IL was found to be the top-ranked gene that was significantly down-regulated in the curcumin group, considering the established pro-fibrotic effect mediated by inflammosome-secreted IL and NLRP3 activation.
We speculated that the anti-fibrosis effect exerted by curcumin was mediated by mitigating IL expression and secretion in cardiac fibroblasts. FIGURE 5. IL plays significant role in curcumin-mediated anti-fibrotic effect screened from mRNA sequencing A.
Volcano plots indicating up-regulated genes and down-regulated genes between two groups. Purple dots represent down-regulated genes, blue dots represent up-regulated genes, and grey dots represent no significant change.
GO signaling pathway enrichment analysis summary from respective groups. Different colors and dot sizes indicate gene number and gene alteration, respectively.
Mutual correlation among all signaling enrichment observations are displayed in D. TABLE 1. Top 10 up and down-regulated genes enriched in inflammation response pathway. NRCF, co-cultured with PBS-treated macrophages with TGF-β, administration vs NRCF, co-cultured with curcumin-treated macrophages with TGF-β, administration.
Previously, we identified IL as a central molecule in mediating LPS-treated macrophage-activated myofibroblast trans -differentiation on NRCF, while curcumin administration significantly ameliorated this process.
Hence, to test whether compensation of IL in NRCF after co-culture reverses the anti-fibrotic effect of curcumin, we constructed an IL overexpression plasmid and transfected it into TGF-β-stimulated NRCF after co-culture with LPS and curcumin double-treated macrophages.
We discovered significantly upregulated IL gene expression and considerable transfection efficacy, as demonstrated by RT-PCR and immunofluorescence Supplementary Figure S2A,B. Furthermore, IL protein expression levels were determined by ELISA in the supernatant collected from NRCF, indicating successful overexpression after plasmid transfection Supplementary Figure S2C.
As expected, IL overexpression in NRCF significantly reversed the curcumin-mediated anti-fibrotic effect, as shown by the expression of fibrotic genes i. FIGURE 6. Summary data of protein expression are displayed in B — E.
EDA-Fibronectin is plotted in B , Periostin is plotted in C , Vimentin is plotted in D and α-SMA in E F-H. Summary data are plotted in G for p -SMAD2 and H for p -SMAD3 I.
Cardiac fibrosis, characterized by intersection and collagen deposition within the cardiac interstitium due to net accumulation of extracellular matrix ECM proteins, is a common pathophysiological manifestation in most myocardial diseases Berk et al.
In general, the extent of fibrotic remodeling is closely associated with adverse organ outcomes. Myocardial fibrosis is not necessarily the primary cause of dysfunction. In many circumstances, cardiac fibrosis is the result of a reparative process that is activated in response to cardiomyocyte injury.
In humans or other adult mammals, quiescent fibroblasts sustained dynamic balance with cardiomyocytes in healthy status; however, these cells have strong potential in repairing injured myocardium; thus, after pathological conditions, loss of a significant number of cardiomyocytes triggers a reparative program, leading to the formation of fibrous tissue.
For example, in acute MI, the sudden death of many cardiomyocytes initiates an intense inflammatory reaction, ultimately leading to the replacement of dead myocardium with a collagen-based scar Frangogiannis, Cardiac fibrosis in response to ischemic injury can be divided into three stages: acute early response, proliferation, and late maturation.
In cultured rat heart fibroblasts, higher gelatinase activity was observed in response to stimulation with IL-1β, and tumor necrosis factor α TNF-α. Interleukin-1β and tumor necrosis factor alpha decreased collagen synthesis and increased matrix metalloproteinase activity in cardiac fibroblasts in vitro , and they also differentially regulated the production of tissue inhibitors of metalloproteinases.
After ischemia reperfusion—induced heart injury, IL-1 receptor 1-deficient mice showed decreased accumulation of macrophages in the infarcted myocardium and diminished early inflammatory and pro-fibrotic responses Bujak et al.
However, extended exposure of cardiac fibroblasts to inflammatory cytokines, such as IL-1β, was observed in the prolonged inflammatory phase post-MI. The long-term action of IL-1 β on cardiac fibroblasts delays or prevents the transition from the pro-inflammatory stage to the proliferative phase of heart repair, which may induce adverse remodeling and heart failure by reducing heart contractility and promoting cardiomyocyte apoptosis Bujak and Frangogiannis, In contrast to IL-1β, TNF-α may indirectly induce the profibrotic activity of fibroblasts by increasing the expression of type 1 angiotensin II AT1 receptors.
Indeed, most inflammatory cytokines that cooperate in the pro-inflammatory activation of cardiac fibroblasts can demonstrate effects on fibrotic fibroblast activity. In our study, we revealed that macrophages secreting IL-1β, TNF-α, and IL-6 play a significant role in mediating cardiac fibroblast trans -differentiation, which is in accordance with the conclusions derived from the aforementioned previous studies.
Curcumin has roles in various cardiovascular diseases, including ischemic heart, pressure overload heart, and metabolic disorder-related cardiac diseases. However, in our study, we did not confirm the therapeutic effect of curcumin directly in cardiomyocytes, which reflected by the fact that no significant change in cardiomyocyte apoptosis was found in curcumin treated group in mice heart 7 days after MI compared with MI only.
In addition, previous studies have also reported that the administration of curcumin in ischemic diseases can salvage the functionality of endothelium Pu et al. The findings illustrated above strongly hints that the regulation of cardiac fibrosis by curcumin may play pivotal role in improving cardiac function after MI.
Although it has been well-validated that curcumin inhibits inflammation and anti-ROS as described previously, in a number of studies, curcumin was reported to be directly associated with collagen deposition and fibroblast proliferation.
This study had several limitations. Second, the polarization of macrophages monocytes post-MI needs to be validated in future studies because both M1 type macrophages which secrete IL-6, IL1β, and TNF-α and M2 type macrophages, which serve as reparative forms post injury, can initiate cardiac fibrosis.
In summary, our study revealed that the administration of curcumin significantly ameliorated inflammation in the acute phase, as reflected by the promotion of macrophage apoptosis, accompanied by decreased pro-inflammatory cytokine secretion, including IL-6, IL1b, and TNF-α.
These findings suggest that curcumin has potential as a potent therapeutic target in treating adverse remodeling in ischemic heart disease. The datasets presented in this study can be found in online repositories. The animal study was reviewed and approved by the second affliated hospital of zhejiang university school of medicine ethics committee.
Written informed consent was obtained from the owners for the participation of their animals in this study. NC organized and designed this study and wrote the manuscript, ZJ orchestrated the whole study and performed data analysis, YC and ZZ did all pathology studies, JH did the flow cytometry experiments, QC and TH helped with the animal model.
All authors contributed to the revision of the manuscript and approved the final version. This work was supported by grants from National Natural Science Foundation of China No. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The handling editor declared a shared parent affiliation with the authors at the time of the review.
Hesrt Chamomile Tea for Stress Relief studies show that turmeric has Diseaes benefits for wnd body and brain. Many of these benefits come from Wild salmon recovery Curcumin and Heart Disease active ingredient, curcumin. The spice known as turmeric could be one of the most effective nutritional supplements in existence. Turmeric is the spice that gives curry its yellow color. It has been used in India for thousands of years as both a spice and medicinal herb.
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