Glutathione for cardiovascular health -
Such nutrients can be supplemented or found naturally in food:. Glutathione Protects More Than Just Your Heart Glutathione is in nearly every cell of your body. It plays an invaluable role in immune function, reduction of the oxidative effects related to everyday metabolic processes, cleansing the blood through neutralization of toxins for disposal in bile, heavy metal detoxification, DNA repair and more.
Speak with your healthcare provider to assess your need for further glutathione support. Therefore, activating GPX4 and GSH to inhibit ferroptosis is an attractive option for cardiac disease therapy Fig.
Identifying strategies that fortify the GSH system in the heart may contribute to developing therapies against cardiac diseases induced by various pathological factors. This section summarizes potential approaches to increasing the GSH system in the heart. The direct administration of GSH in vivo is probably an obvious way to increase GSH It has been demonstrated that modified oral glutathione-like liposomal GSH increases erythrocyte and plasma GSH levels and reduces oxidative stress biomarkers [ 98 ].
Moreover, other routes of administration, such as intravenous, intranasal, and sublingual administration, can increase GSH levels [ 99 ]. However, the direct administration of GSH is rare in myocardial injury treatment studies.
In addition, supplementing the raw materials cysteine, glycine, glutamate, and selenium for synthesizing GSH or GPX to achieve an elevated GSH system in the myocardium is another feasible strategy. Next, we review the evidence supporting that increased raw material availability causes high GSH and GPX levels in the myocardium Table 1 , Supplementary Table S1.
N-acetylcysteine NAC is a precursor of the amino acid cysteine. NAC deacetylates under the action of N-deacetylase to enhance intracellular Cys, thereby increasing the endogenous synthesis of GSH. In , Rafeek HidhayathBasha et al.
conducted a study on the protective effect of NAC on isoproterenol ISO -induced MI in rats [ ]. The results demonstrated that pretreatment with NAC not only significantly increased the activities of GSH and GPX but also reduced the levels of lipid peroxidation in the heart mitochondria of ISO-treated rats [ ].
Interestingly, NAC exerts a GSH-supplementing effect in GSH-deficient cells, whereas this effect may be ineffective in GSH-enriched cells [ ]. In humans, clinical studies have evaluated the effects of NAC treatment on myocardial infarction.
M A Arstall et al. The results indicated that patients treated with NAC had a 5. Therefore, NAC can be used to boost cardiac GSH levels and attenuate myocardial injury. Apart from NAC, whey protein and methionine are also precursors of Cys.
Whey protein and its concentrates are abundant in sulfur-containing amino acids such as Cys and methionine, so it can supplement cysteine and efficiently improve GSH levels [ 99 , ]. Researchers do not recommend methionine because it causes an increase in homocysteine levels [ 99 ].
Elevated homocysteine is associated with various diseases, such as heart and brain diseases. Severe hyperhomocysteinemia in patients is able to develop neurological and cardiovascular disorders as well as premature death owing to complications [ ]. A study revealed that L-methionine supplementation 1.
O for 8 weeks was sufficient to produce hyperhomocysteinemia in rats and markedly increased the mean arterial pressure, oxidative stress and mean cardiomyocyte diameter [ ]. Glycine Gly is another essential amino acid in the synthesis of GSH.
Although most studies have focused on increasing cysteine levels in vivo to boost GSH synthesis, glycine supplementation alone or in combination with NAC to increase GSH synthesis has also attracted extensive attention.
In a burn rat model, intraperitoneal injection of glycine supplementation alleviated severe burn-induced cardiac injury by improving cardiomyocyte energy metabolism and increasing ATP and GSH contents [ ].
Premranjan Kumar et al. They also clarified in another clinical study that supplements with glycine 1. Gln acts as a precursor of glutamate Glu , equivalent to being an indirect glutathione precursor.
Its supplementation can enhance intracellular GSH levels and provide protection against myocardial injury. In ISO-induced myocardial infarction, pretreatment with Gln maintained cardiac GSH kurtosis and antioxidant enzyme GPX, SOD, CAT activity at near-normal levels, thus preventing oxidative damage in the myocardium [ ].
A separate experiment elucidated that Gln supplementation increased cardiac GSH to halt myocardial injury induced by cyclophosphamide CPA in rats [ ]. Notably, there is a significant correlation between plasma Gln concentrations and GSH levels. A double-blind, randomized, placebo-controlled trial demonstrated that perioperative high-dose intravenous injection of Gln 0.
O for 3 days raised plasma Gln concentrations and maintained plasma GSH levels in postoperative patients undergoing cardiopulmonary bypass CPB [ ]. Selenium Se is an essential trace element for humans and animals, serving as the main component of many antioxidant proteins in the body, such as thioredoxin reductase, selenoprotein P and GPX.
As a result, selenium may play an important role in protecting cardiomyocytes from oxidative stress [ ]. Compared with a low-Se diet 0. Zhu et al. showed that Se boosted GPX1 expression by inhibiting DNMT2-mediated DNA methylation of the GPX1 promoter from lessening ROS production in advanced glycation end-product AGE -induced heart failure [ ].
In humans, a systematic review and meta-analysis revealed that physiologically high selenium levels in the body were negatively associated with cardiovascular disease morbidity and mortality.
In addition, there is a U-shaped association between selenium exposure and some diseases, such as type 2 diabetes and fractures [ ]. However, it has also been reported that selenium supplementation alone is not associated with cardiovascular disease and all-cause mortality [ ].
Other than providing raw materials for the GSH system, another antioxidant strategy that activates the glutathione system is often achieved through medicinal therapy.
In this section, we will describe their effects and mechanisms in detail by the source of the drugs. Natural medicines have been a reliable source of drugs since ancient times, playing an essential role in preventing and treating various diseases.
At present, increasing evidence has shown that compounds derived from natural medicines exert a variety of beneficial effects, including antioxidant, anti-inflammatory, and anti-apoptosis effects [ , , ].
To date, more than natural medicine monomers have been reported to activate the GSH system by several mechanisms to protect the heart from oxidative stress. Next, we will summarize some promising medicine monomers that activate the GSH system based on the categories of natural medicines, including flavonoids, terpenoids, phenolic acids, quinones, and alkaloids Table 2 , Supplementary Table S2.
Flavonoids are a group of phytochemicals widely existing in nature. They have received extensive attention for their antioxidant, anti-inflammatory, anti-mutagenic and anti-cancer properties, as well as their ability to protect against cardiovascular disease [ ].
Quercetin Quer is one of the main flavonoids in many vegetables and fruits. It not only abrogates cardiac oxidant stress but also alleviates the inflammatory response and deterioration of heart function in MIR injury and DCM in rodents [ , ].
O for 8 weeks evidently improved serum total antioxidant capacity TAC in postmyocardial infarction patients compared to the placebo group [ ]. O for 2 mouths to standard therapy improved cardiac function both systolic and diastolic functions and reduced the total duration and number of ST-segment depressions in patients with coronary heart disease CHD [ ].
Thus, Quer, as an activator of the GSH system, is a promising natural small molecule for the treatment of cardiac injury. Catechins, known as dihydroflavonols, are natural flavonoids present in green tea and other beverages, including catechin, epicatechin EC , and epigallocatechingallate EGCG [ , ].
It has been reported that these three compounds can enhance the contents of GSH and the activities of GSH-dependent antioxidant enzymes GPX and GST and reduce lipid peroxidation and cardiac damage mediated by DOX or isoproterenol ISO in the myocardium of rats, respectively [ , , ].
Genistein is the main ingredient of isoflavone from soybean and is also used as a tyrosine kinase inhibitor. It has potent effects of antioxidant, anti-inflammatory, anti-angiogenesis, and anti-cancer [ ]. Studies have shown that genistein can increase GSH levels and GPX activity along with decreased oxidative stress in diabetic cardiomyopathy and DOX-mediated cardiomyopathy [ , ].
Meanwhile, genistein increased the levels of Nrf2, which is vital to the GSH system [ , , ]. However, it is unclear why genistein upregulates the levels of Nrf2 in the myocardium. O for one year improved both cardiac function and left atrial remodeling in postmenopausal women with metabolic syndrome [ ].
O for 24 weeks significantly increased the protein and mRNA levels of Nrf2 and the concentrations of SOD as well as diminished serum levels of inflammatory factors and MAD in patients with myocardial ischemia [ ].
Therefore, genistein, an antioxidant, might be a potential drug for treating patients with myocardial injury. Terpenoids are natural compounds with a wide distribution, great variety, and diversified structure in nature [ ].
Terpenoids have been reported to activate the GSH antioxidant system to protect the heart from oxidative stress and alleviate cardiac injury. Tetraterpenes, also called carotenoids, are widespread in higher plants, fungi, algae, and animals and are one of the most potent natural antioxidants [ ].
It could also alleviate the size of myocardial infarction and the subsequent decrease in cardiac function in rats [ ]. A clinical study of patients with myocardial infarction by B Panczenko-Kresowska et al.
revealed that β-carotene supplementation remarkably diminished plasma lipid peroxide levels in patients [ ]. The mechanism might be related to its own antioxidant properties and GSH activating effect. Nonetheless, the most updated literature reports that β-carotene supplementation or elevated blood β-carotene levels may increase all-cause mortality and CVD risk [ , ].
O for 2 months , was reported to significantly increase the ratio of serum TAC to MDA in patients with type 2 diabetes [ ]. In addition, tanshinone IIA Tan IIA is a diterpene extracted from the root and rhizome of Salvia miltiorrhiza Bunge.
Its water-soluble derivative, sodium Tan IIA sulfonate injection STS , is widely used in the clinic as an adjuvant drug for coronary heart disease, myocardial infarction and heart failure in China [ ].
Tan IIA induced activation of the GSH system to attenuate cardiac oxidative stress and restrain the increase in serum myocardial enzymes, thus relieving the extent of myocardial damage [ , ].
Moreover, a meta-analysis showed that the addition of STS seemed more effective in treating heart failure than Western medicine alone [ ].
The excellent clinical manifestations of Tan IIA provide supportive evidence for targeting the GSH system in the treatment of heart diseases, which may be promising for transforming natural compounds from basic research to clinical applications.
Phenolic acids are attracting increasing attention for their antioxidant properties and other health benefits. Based on differences in the carbon skeleton, phenolic acids can be mainly divided into two categories: hydroxycinnamic acid e. All of the compounds above have been proven to maintain GSH contents and GSH-dependent antioxidant enzyme activities in the myocardium, protecting it from oxidative stress [ 41 , , , , , , , ].
Ferulic acid FA , the main active component isolated from Angelica sinensis , has been documented to increase the levels of GSH and the expression of GPX in the myocardium by upregulating AMPKα2 and activating Nrf2 signaling [ 41 , ]. In recent years, ferulic acid derivatives have been widely investigated.
Of them, sodium ferulate SF features low toxicity, stability, ease of synthesis, and water solubility and has been authorized by the State Drug Administration of China as an adjuvant drug for treating ischemic cardiovascular diseases [ , ].
It could also increase GPX activity, thereby exerting antioxidative effects in rats [ ]. Besides, caffeic acid and chlorogenic acid caffeoylquinic acids are two other classical phenolic acids widely found in natural plants, both of which are the most vital active substances in coffee [ ].
Some investigations have demonstrated that the two compounds, acting as agonists of the GSH antioxidant system, well prevent oxidative stress and reduce heart damage in some animal cardiomyopathy models, for instance, the ISO-induced myocardium infarction model [ , ].
Additionally, one clinical study reported that consumption of chlorogenic acid-enriched coffee not only improved plasma antioxidant capacity and decreased plasma lipid and protein oxidation but also donated to enhancing cardiovascular health in people with hypercholesterolemia [ ].
Interestingly, Yuki Sato and coworkers indicated that the antioxidant effect of caffeic acid is more potent than chlorogenic acid, and the latter is metabolized into caffeic acid in the intestine. Ellagic acid EA also increased the GSH antioxidant system and diminished oxidative stress in several models of myocardial injury, such as diabetes and cisplatin-mediated heart injuries [ , ].
O for 8 weeks significantly fortified the mean of TAC and the activity of GPX enzymes as well as reduced MDA contents in the serum of type 2 diabetic patients [ ]. Nonetheless, it is not certain whether EA may be helpful in boosting the GSH system in cardiac patients and treating heart diseases.
Thus, there is a need for larger studies to fully address this issue. In addition, EA was found to have poor low oral bioavailability, thus limiting its clinical applications. In contrast, its intestinal microbial metabolite, urolithin, possesses better biological activity and higher bioavailability [ ].
It has been reported that urolithin A also increased total GSH, lowered oxidative stress, and improved cardiac function in the myocardium of diabetic rats [ ]. Coenzyme Q10 CoQ10 is a fat-soluble quinone.
It is also a natural antioxidant molecule in the body. The positive effect of CoQ10 treatments is recognized in patients with heart failure and myocardial ischemia, such as the reduction of oxidative stress derived from cardiovascular causes, decrease in mortality and hospitalization and improvement in cardiac function [ , ].
Thereinto, the antioxidant effect of CoQ10 may be partially attributed to activating the GSH system. In a rat model of ISO-mediated myocardial infarction, CoQ10 preconditioning not only markedly expanded cardiac GSH levels and reduced the concentration of lipid peroxidation but also alleviated myocardial damage [ ].
O for 12 weeks on the antioxidant system in patients with coronary artery diseases. The findings revealed that plasma GPX activity was significantly increased after CoQ10 therapy and was positively related to plasma coenzyme Q10 levels [ ]. Thymoquinone Thy , a benzoquinone compound, is the main active ingredient in the extract of Nigella sativa seeds.
Its treatment was reported to increase the levels of GSH and the activities of GPX and GST, along with a decrease in cardiac lipid peroxide production in a rat model of myocardial injury caused by diazinon a pesticide [ ]. Moreover, Thy-rich Nigella sativa seed oil exerts an antioxidant effect as an adjuvant therapy in hypertensive patients, mainly manifested in the upregulation of serum glutathione reductase GR levels and reduction of serum MAD content.
It also showed beneficial impacts on glycemic and blood pressure control as well as lipid metabolism in hypertensive patients without serious adverse effects such as liver and kidney dysfunction [ ].
In addition, some quinone compounds, such as β-LAPachone and aloin, have similar effects on heart protection [ , ]. We will not give unnecessary details here. In addition to the above compounds, many other natural medicines potentially protect the myocardium by enhancing the GSH antioxidant system.
Curcumin is a classic curcuminoid extract from the rootstock of turmeric. Upstream molecular targets, such as Nrf2, Sirt3, and PPAR-γ, are responsible for the curcumin-enhanced GSH system [ , , ]. Moreover, curcumin treatment not only quells oxidative stress in the myocardium but also impedes myocardial inflammation, which improves heart function and decreases heart damage [ , , , , ].
O for 12 weeks in patients with CHD [ , ]. Considering that curcumin is nontoxic, readily available and inexpensive, it is a prospective candidate for treating heart diseases. Resveratrol RSV is a stilbene found in grapes, wine and blueberries that possesses potent antioxidant activity to protect the myocardium from oxidative damage.
In particular, the enhanced GSH system plays an essential role in the antioxidant capacity of RSV [ ]. In , Elif Tatlidede et al.
demonstrated that RSV treatment notably raised cardiac GSH contents and suppressed oxidant responses in DOX-processed rats; Simultaneously, it ameliorated DOX-induced deterioration of cardiac function and myocardial injury [ ].
In the following decade, many researchers verified in various models of myocardial injury that RSV can exert an antioxidant effect and protect the myocardium by increasing the level of GSH and upregulating the activity of GSH-dependent antioxidant enzymes [ , , , , ]. Moreover, they revealed that the mechanism by which RSV enhances the GSH system involves the AMPK signaling pathway, the Nrf2 signaling pathway, the Sirt1 pathway, noncoding RNA miR and the KAT5 gene [ , , , , ].
O for 2 months better improved left ventricular ejection fraction and left ventricular diastolic function in patients with CHD compared with standard treatment alone [ ].
Synthetic drugs have been researched and developed in recent modern times, a proportion of which have already been in clinical use for the treatment of various diseases, such as myocardial infarction, heart failure, diabetes, hypertension, oncology, and sepsis.
Similar to natural drugs, many synthetic drugs have properties that enhance the GSH system and thus protect cells from oxidative damage. The following section describes and summarizes these drugs in terms of the mechanisms by which they activate the GSH system Table 3 , Supplementary Table S3.
The key upstream target for GSH system modulation is generally considered to be Nrf2, a redox-sensitive regulator. Nrf2 is involved in not only the regulation of GSH synthesis and reduction via upgrading some enzymes and proteins SLC7A11, GCLM, GCLC, GR but also the activation of GSH-dependent antioxidant enzymes GPX, GST [ , ].
Furthermore, Gobinath Shanmugam et al. revealed that in an ISO-mediated model of myocardial infarction, direct overexpression of the Nrf2 gene enhanced GSH levels in cardiomyocytes and guarded cardiomyocytes against oxidative damage and lessened the occurrence of ferroptosis [ ].
This further confirms that the enhancement of Nrf2 is a viable strategy for activating the GSH system. Melatonin prevents Nrf2 degradation and augments its nuclear accumulation by inhibiting proteasomal [ ].
In in vivo and in vitro studies, melatonin was proven to increase the level of Nrf2 in cardiomyocytes exposed to oxidative stress. Among them, Cai et al. revealed the grievous connection between oxidative stress, pyroptosis, inflammation response, and xenobiotic metabolism in the myocardium of TMT-treated rats by String database analyzing the proteome interaction protein [ ].
In addition, Shaghayegh Haghjooy Javanmard et al. O for 30 days notably raised Nrf2 levels in peripheral blood mononuclear cells of patients undergoing coronary artery bypass grafting CABG [ ]. O for 12 weeks increased serum GSH levels while reducing serum MDA and protein carbonyl PCO in CHD patients with type 2 diabetes.
Additionally, it was reported that trimetazidine TMZ , a piperazine derivative, mediated activation of the GSH system and had antioxidant and cytoprotective effects in several myocardial injury models [ , , , ].
For instance, in the myocardium of exhaustive-exercised rats, TMZ produced specific cardioprotective outcomes by increasing GSH and GPX activity to clear oxidative stress. Further mechanistic studies have found that treatment with TMZ promoted cardiac Nrf2 expression, indicating that TMZ enhanced the clearance of oxidative stress by activating the GSH system through the Nrf2 signaling pathway [ ].
Moreover, TMZ also has other benefits to the myocardium, including increased coronary blood flow reserve, maintenance of cardiac energy metabolism, anti-apoptosis, and anti-inflammation. It has been approved for clinical use in the therapy of angina pectoris [ , ]. In addition to Nrf2, activation of PPAR-γ and the AMPK pathway can also facilitate the GSH system.
Rosiglitazone and pioglitazone belong to the thiazolidinedione class of hypoglycemic agents and are recognized as PPAR-γ agonists.
O for 4 weeks exhibits antioxidant properties in diabetic patients, as reflected by a decrease in MDA [ , ]. In addition, there is evidence that pioglitazone reduces the risk of MI and acute coronary syndrome in patients with cardiovascular diseases CVD and patients with type 2 diabetes who had previous myocardial infarction [ , , ].
Notably, it increases the risk for the development of heart failure [ , ]. Compared to pioglitazone treatment, rosiglitazone increases the risk of AMI and heart failure in type 2 diabetic patients and elderly patients [ , , ].
Metformin is a traditional drug for the treatment of type 2 diabetes. In addition to its antidiabetic results, it was also found to achieve cardiac protection by activating the AMPK pathway [ ].
Some researchers have shown that metformin activates AMPK and triggers the downstream GSH system to slow DOX-mediated oxidative impairment in the myocardium [ , ]. O for 12 months not only decreased oxidative stress but also lowered left ventricular mass LVM and improved blood pressure [ ].
SLC7A11 is an essential molecule that limits the Cys transport rate, thus restricting the synthesis of GSH. Direct SlC7A11 overexpression in cardiac myocytes boosted GSH levels and reduced cardiac ferroptosis and injury, suggesting that it is feasible to fortify GSH levels by increasing SLC7A11 [ 76 ].
Atorvastatin, a statin that reduces cholesterol, is a first-line drug for treating cardiovascular disease. It was reported that it could raise intracellular GSH by increasing SLC7A11 expression, efficiently leading to GPX4 enhancement and ferroptosis suppression in the ISO-induced injury model of H9C2 cells and rat myocardium [ 49 ].
Additionally, one clinical trial by Douglas Greig et al. O for 4 weeks reduced plasma MDA while improving the functional capacity assessed via a 6-minute walk test in patients with chronic heart failure CHD [ ]. However, it is not clear whether they regulate the expression of SLC7A Dexmedetomidine DEX , an α2-adrenergic receptor, also augments the expression of SLC7A In the same year, Wang et al.
Moreover, DEX treatment 0. A previous clinical study also showed that perioperative DEX 0. These results suggest that DEX has antioxidant and cardioprotective potential. However, clinical studies of the drug have focused on surgical patients. It is unclear whether it exhibits cardioprotective effects in patients with post-PCI, AMI, or other cardiomyopathies.
Many studies have concentrated on the direct effects of synthetic drugs on GSH and GSH-dependent antioxidant enzymes in damaged myocardium without further mechanistic investigations.
Herein, we discuss some critical examples of representative synthetic compounds. Captopril, an angiotensin-converting enzyme inhibitor, is widely used in clinical practice to treat hypertension, MI, and congestive heart failure and is effective in attenuating left ventricular LV dilatation, ameliorating LV ejection fraction and improving cardiovascular morbidity and mortality [ , ].
Captopril has been revealed to facilitate the GSH system in several rodent models of myocardial injuries, such as clozapine and DOX-induced damage models, thereby protecting cardiomyocytes from oxidative stress [ , ].
A recent clinical trial in type 2 diabetes patients with CVDs following captopril treatment O for 3 months found a significant improvement in plasma GSH levels and a concomitant decline in lipid peroxidation [ ]. Consequently, these results partially explain the pharmacological mechanism of captopril as a cardioprotective agent.
Similar to the statin lipid-lowering drugs mentioned earlier, other lipid-lowering drugs, such as probucol, also exhibit the capability to restore the inhibited GSH system and defend the myocardium from oxidative damage after exposure to pathological factors, for example, ISO and cyclophosphamide [ , ].
Exosomes EXOS of mesenchymal stem cells MSCs from human umbilical cord blood increased GSH and attenuated lipid peroxidation and ferroptosis in cardiomyocytes in a rat infarction model. However, it has no effect on the level of GPX4 [ ].
A recent study reported that exosomes derived from mouse bone marrow MSCs exerted similar cardio-protective effects [ ]. However, not all exosomes positively impact the myocardium and GSH.
For instance, exosomes secreted by adipose tissue macrophages caused ferroptosis by targeting SLC7A11 to inhibit GSH synthesis in the heart [ ].
Current gene therapy research aims to target, for example, upstream targets of the GSH system or molecules associated with it such as Nrf2, GPX, SLC7A11 , genes aberrantly expressed in myocardial injury, and noncoding RNAs regulating mRNA transcription [ 76 , , , , , ].
Recombinant human GPX4 alleviated ISO-induced myocardial ischemia injury [ ]. In addition, some investigators found that USP22 and lncRNA PART1 expression was decreased in a MIR injury model. In addition, Zhang et al. overexpressed miRp in the myocardium by direct myocardial injection of AVV-9 containing miRp precursor, which targeted inhibition of MyD88 and thus restored declining GSH levels, alleviated insult of cardiac function and oxidative injury induced by sepsis in the hearts of mice [ ].
The GSH system is one of the most significant members of the cellular antioxidant defensive system, which is essential for eliminating excess ROS and protecting the myocardium in the presence of pathological cardiovascular factors.
Notably, glutathione balance and GPX4 levels are deeply involved in the susceptibility of cardiomyocytes to ferroptosis, a novel form of cell death.
Furthermore, many researchers have found that reduced GSH levels and GSH-dependent antioxidant enzyme activity in damaged myocardium due to excess ROS and disruption of the GSH synthesis process, along with increased oxidative damage and ferroptosis.
Based on this, therapeutic strategies to restore the activity of the GSH system in the heart are beneficial in the treatment of myocardial injury.
Precursors of GSH or GPX biosynthesis, various small molecule activators related to the GSH system and some novel therapeutic approaches, such as exosomes and gene therapy, can boost the activity of the GSH system and reduce cardiac damage and ferroptosis.
Notably, despite constant progress in diverse aspects of natural drug monomers that protect against myocardial injury by activating the GSH system, great challenges remain in translating these compounds into future clinical pharmaceuticals.
First, most natural small molecules present low bioavailability problems [ ], so further research on delivery systems and formulations for these drugs is needed. Second, the development of new drugs requires additional and more detailed preclinical and clinical studies to determine whether long-term use is biotoxic, whether the drug has adverse effects on other peripheral organs or whether the drug candidate has a real therapeutic effect on the patients.
In addition, a portion of synthetic agents have been used clinically to treat various diseases, such as myocardial infarction, heart failure, diabetes, hypertension, tumors, and sepsis. These studies on myocardial injury and the GSH system reveal new roles of these clinical drugs in the treatment and further elaborate their mechanisms, which provide new ideas for their clinical application.
However, more clinical studies must be encouraged to evaluate whether these drugs can act as GSH system enhancers and cardioprotective agents in patients. Moreover, some emerging therapeutic approaches to enhance the GSH system have attracted much attention.
These results show that although the expected therapeutic effect has not been achieved, AVV-based therapy has acceptable safety. This opens up the possibility of our gene therapy targeting the GSH system. Overall, we can see the value of targeting the GSH system in myocardial injury.
Despite being faced with many problems, it provides new directions and ideas for the treatment of myocardial injury. The continuous exploration of new treatment modalities will be critical to successfully combat myocardial damage in the future. All data generated or analyzed during this study are included in this published article and its supplementary information files.
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Citation: Strutynska N, Goshovska Y, Mys L, Strutynskyi R, Luchkova A, Fedichkina R, Okhai I, Korkach Y and Sagach V Glutathione restores the mitochondrial redox status and improves the function of the cardiovascular system in old rats. doi: Received: 08 November ; Accepted: 22 December ; Published: 09 January Copyright © Strutynska, Goshovska, Mys, Strutynskyi, Luchkova, Fedichkina, Okhai, Korkach and Sagach.
Introduction: Cardiovasculat is Glutathionf by cardiovascular heaoth which is associated with an imbalance of hewlth and antioxidant systems, the mitochondrial dysfunction, etc. Glutathione GSH plays Fat burner reviews critical role in protecting Gkutathione Quick snack ideas oxidative damage. The Glutathione for cardiovascular health of cardjovascular work was to study the effect of Cauliflower and corn chowder glutathione Glutathione for cardiovascular health the redox status of mitochondria, the content of H 2 S and the function of the cardiovascular system in old rats. Methods: Experiments were performed on adult 6 months and old 24 months Wistar rats divided into three groups: adult, old and glutathionetreated old rats. Results: Our data shows that in old rats treated with glutathione, the balance of its oxidized and reduced form changes in the direction of a significant increase by At the same time, in glutathione-treated old rats, we also observed restoration of endothelium-dependent vasorelaxation responses to acetylcholine, which were almost completely abolished by the NO-synthase inhibitor L-NAME. Thank you ehalth visiting nature. You Quick snack ideas using a Acrdiovascular version with BMI for Public Health support for CSS. To obtain the best experience, we recommend Glutathione for cardiovascular health use a cardiovzscular up Cardiovascularr date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. The glutathione GSH system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species ROS.
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