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All mice launched at the same place and time, and the number of crossing target quadrant and the original platform area were observed. Data were collected by an online video tracking device RDMWM-G, Moblie Datum Inc, Shanghai, China. We verified mice death by respiratory and cardiac arrest.
Brains were rapidly removed from the cerebrum of the mice, and the best efforts were made to minimize animal suffering. One part of brains was snap frozen using liquid nitrogen, and then stored at 80 °C for enzyme-linked immunosorbent assay ELISA and Bicinchoninic acid analysis.
Paraffin-embedded brain tissue was cut into 5 µm sections from optic chiasma to cerebral transverse fissure on a microtome, following deparaffinization in xylene and rehydration with graded ethanol. Protein levels of interleukin-1β IL-1β and interleukin-4 IL-4 in the hippocampus and prefrontal cortex were measured to investigate the regional response of pro-inflammatory and anti-inflammatory cytokine of mice by ELISA kit Beyotime, Shanghai, China.
Briefly, serial dilutions of protein standards and samples of mice were added to ELISA plates, followed by biotinylated anti-IL-1β and IL-4 antibody addition. Then, the prepared solution of avidin-horseradish peroxidase conjugate complex was added, and the unbound conjugates were washed away with phosphate buffered saline.
The reaction was stopped by adding stopping solution, and absorbance was read at nm. To further determine whether AST influences anti-oxidation, we analyzed SOD activity and MDA content in the hippocampus and prefrontal cortex of each group.
All hippocampus tissue were obtained after normal perfusion 0. A 10 mg hippocampus tissue was weighed and added to ml SOD sample preparation fluid. The mixture was homogenized at 4 °C or ice bath. Then supernatants were obtained and used as a sample to be tested after centrifugation at 12, g for 3—5 min at 4 °C.
Bicinchoninic acid kit used to determine the protein concentration of each sample, and SOD and MDA tests were performed according to kits steps Beyotime, Shanghai, China [ 18 ].
All data were statistically analyzed with SPSS During the period of dministration, the average body weight of each group increased steadily for 30 days, except for slight fluctuations in the first ten days.
Taken together, these data indicated that AST could improve the non-spatial cognitive function in mice with VD. The discrimination index of different groups, with 13 mice per group. As shown in Fig. These findings indicated that AST might ameliorate the impairment of spatial acquired function to a certain extent.
The results of morris water maze test, with 13 mice per group. a The average escape latency period of every group in the five days. b The path length of each group in the five days. c Time for mice crossing platform quadrant. Results showed that the hippocampal neuron structure in LUCCAO-treated mice was significantly damaged, and their nuclei was lost Fig.
In particular, the neurons in the hippocampal CA1 and CA3 area of mice in model group contracted seriously and the adjacent gap were enlarged, with disordered and hyperchromatic arrangement of neurons. After AST treatment, the damage of neuron was alleviated, and the neurons in CA1 and CA3 areas were remarkably improved, with orderly arrangement and large and clear nucleus.
These findings indicated that AST could alleviate the morphological impairment caused by VD in mice. IL-1β level in the LUCCAO-treated mice was significantly elevated compared to that in sham group in the hippocampus and cerebral cortex. The expression of IL-1β and IL-4 in the hippocampus and prefrontal cortex of each group mice, with 13 mice per group.
a The expression of IL-1β in the hippocampus. b The expression of IL-1β in the prefrontal cortex. c The expression of IL-4 in the hippocampus. From Fig. These findings clarified that AST could inhibit the level of oxidative stress.
SOD activity and MDA content in the hippocampus and prefrontal cortex of each group, with 13 mice per group. a The value of SOD activity in the hippocampus. b The value of SOD activity in the prefrontal cortex. c The level of MDA in the hippocampus. The most significant finding of this study was that AST ameliorated the cognitive function and hippocampal neuron in VD mice, which may be associated with the inhibition of inflammatory response and oxidative stress, revealing that the potential value of AST in the treatment of VD.
Currently, many VD animal models have been established, among which 2VO rat model is a classic VD model of whole cerebral ischemia. Numerous studies have shown that permanent hypoxia and hypoperfusion of brain induced by bilateral common carotid arteries 2VO in rat model can lead to VD and oxidative stress of brain neurons, and ultimately cholinergic dysfunction and decreased learning and memory ability [ 21 , 22 ].
However, 2VO is only limited to rats and is not suitable for mice, because rats have a complete circle of Willis. Mice lacking complete circle of Willis will suffer from severe ischemia and even death if perform 2VO [ 23 ]. Recently, UCCAO model is adopted for VD mice model, which is modified from 2VO model [ 24 ].
In this study, we established VD mice model induced by LUCCAO. Due to the complex pathogenesis of VD-related cognitive dysfunction, there is still no effective treatment. Therefore, it is necessary to find a specific and effective therapeutic drug. Recent studies have shown that AST has the effect of anti-inflammation, anti-apoptosis, anti-oxidation, anti-aging, anti-tumor, and boosting immunity [ 26 , 27 ].
In the central nervous system CNS , AST is regarded as a potential neuroprotective drug because of its powerful antioxidant property [ 28 ].
In this study, AST alleviated cognitive dysfunction and hippocampal structural damage to a certain extent, indicating that AST had therapeutic effects on VD cognitive dysfunction.
In addition, many previous studies have shown that AST can be used as a protective agent in ischemia model owing to its antioxidant potential [ 29 , 30 ], which is consistent with this study. It has been demonstrated that inflammatory response and oxidative stress are involved in VD-related cognitive impairment [ 31 , 32 ].
Overexpression of inflammatory factors can lead to neuron damage in the hippocampus, thus affecting the cognitive function of mice [ 33 ]. Miao et al. have confirmed that the levels of interleukin-6 IL-6 , tumor necrosis factor-a, and COX-2 are increased in the brain tissue of type 2 diabetes mellitus rats with cognitive dysfunction [ 34 ].
Research conducted by Paloma Bermejo et al. The above studies demonstrate that inflammatory cytokines play a role in the pathogenesis of cognitive dysfunction. In the present study, we found that pro-inflammatory cytokine IL-1β level was increased, while anti-inflammatory IL-4 level was decreased in VD mice, which was consistent with the view that inflammatory cytokines were associated with the pathogenesis of VD-related cognitive dysfunction.
However, AST treatment remarkably lowered the IL-1β expression and enhanced IL-4 expression in the hippocampus and prefrontal cortex, indicating that the alleviation of AST in cognitive impairment may correlated with suppression of inflammatory response.
Under normal and non-stress conditions, oxidation and antioxidants levels are relatively balanced, but are out of balance under harmful external stress, thereby leading to the mass production of reactive oxygen species and the relative shortage of antioxidants [ 36 ].
Subsequently, a large amount of reactive oxygen species in the organism results in the formation of MDA. MDA is a vital indicator of lipid peroxidation and reflects the severity of oxidative stress injury [ 37 ].
In addition, as a free radical scavenger, SOD can protect brain tissue from oxidative stress damage [ 38 ]. Mamun et al. have also confirmed that ATX can inhibit neuronal oxidative stress caused by aluminum chloride and ameliorate spatial memory impairment in mice [ 39 ].
In this current study, MDA production was elevated and SOD activity was diminished in the hippocampus and prefrontal cortex after LUCCAO, which were significantly reversed by AST treatment. Therefore, we hypothesized that ATX could play a neuroprotective role in cognitive dysfunction of VD mice through its antioxidant effect.
Oxidative stress caused by VD can damage the structure of neurons. The results of this study presented damaged hippocampal neuron structure and less nucleus in VD mice, which were alleviated by ATX, indicating that ATX might play a neuroprotective role through anti-oxidative stress and reduced the hippocampal injury of VD mice.
There are some limitations of the study. AST may reduce the damage of neurons in hippocampus induced by VD through oxidative stress, but the apoptosis of neurons was not detected. Besides, we did not detect VD markers such as SB, C-reactive protein and IL Further studies on these issues were required to carried out.
In summary, this study proves the existence of behavioral impairment in VD mice. Additionally, AST has a significant protective effect on VD mice induced by LUCCAO, which can reduce oxidative stress and enhance the inflammatory levels in a dose-dependent manner.
Kalaria RN. Acta Neuropathol. Article PubMed PubMed Central Google Scholar. Venkat P, Chopp M, Chen J. Models and mechanisms of vascular dementia. Exp Neurol. Krenk L, Rasmussen LS, Kehlet H. New insights into the pathophysiology of postoperative cognitive dysfunction.
Acta Anaesthesiol Scand. Article CAS PubMed Google Scholar. Head E. Oxidative damage and cognitive dysfunction: antioxidant treatments to promote healthy brain aging. Neurochem Res. Li MY, Liu XY, Xia CG, Wang GQ, Zhang DM. Astaxanthin enhances hematology, antioxidant and immunological parameters, immune-related gene expression, and disease resistance against in Channa argus.
Aquac Int. Article CAS Google Scholar. Siangcham T, Vivithanaporn P, Sangpairoj K. Anti-migration and invasion effects of astaxanthin against A human glioblastoma cell line.
Asian Pac J Cancer Prev. Article CAS PubMed PubMed Central Google Scholar. You JK, Kim YA, Yokozawa T. Protection against oxidative stress, inflammation, and apoptosis of high-glucose-exposed proximal tubular epithelial cells by astaxanthin. J Agric Food Chem. Sila A, Ghlissi Z, Kamoun Z, Makni M, Nasri M, Bougatef A, et al.
Astaxanthin from shrimp by-products ameliorates nephropathy in diabetic rats. Eur J Nutr. Article PubMed CAS Google Scholar. Hussein G, Nakamura M, Zhao Q, et al. Antihypertensive and neuroprotective effects of astaxanthin in experimental animals.
Biol Pharm Bull. Lu YP, Liu SY, Sun H, Wu XM, Li JJ, Zhu L. Neuroprotective effect of astaxanthin on H 2 O 2 -induced neurotoxicity in vitro and on focal cerebral ischemia in vivo.
Brain Res. Valério Romanini C, Dias Fiuza Ferreira E, Correia Bacarin C, Verussa MH, Weffort de Oliveira RM, Milani H. Behav Brain Res. Article PubMed Google Scholar. Ma J, Yan H, Wang R, Bo S, Lu X, Zhang J, et al.
Protective effect of carnosine on white matter damage in corpus striatum induced by chronic cerebral hypoperfusion. Neurosci Lett. Tripathi DN, Jena GB. Astaxanthin inhibits cytotoxic and genotoxic effects of cyclophosphamide in mice germ cells. Ji X, Peng D, Zhang Y, Zhang J, Wang Y, Gao Y, et al.
Astaxanthin improves cognitive performance in mice following mild traumatic brain injury. Luján M, Castro-Zavala A, Alegre-Zurano L, Valverde O. Repeated Cannabidiol treatment reduces cocaine intake and modulates neural proliferation and CB1R expression in the mouse hippocampus.
Félix H, José B, Carmen G, Jesús A, Lucas JJ. Spatial learning deficit in transgenic mice that conditionally over-express GSK-3beta in the brain but do not form tau filaments.
J Neurochem. Google Scholar. Bromleybrits K, Deng Y, Song W. J Vis Exp Jove. Li X, Qi M, Li C, Dong B, Wang J, Weir MD, et al. Novel nanoparticles of cerium-doped zeolitic imidazolate frameworks with dual benefits of antibacterial and anti-inflammatory functions against periodontitis.
J Mater Chem B. Wu D, Han R, Deng S, Liu T, Zhang T, Xie H, et al. Int J Radiat Oncol Biol Phys. The pathology and pathophysiology of vascular dementia. Plaschke K. Aspects of ageing in chronic cerebral oligaemia.
Mechanisms of degeneration and compensation in rat models. J Neural Transm. Shao Y, Lai XS, Guan CW, Xie LL, Wu LN, Tang CZ. Effect of electroacupuncture on learning-memory ability of vascular dementia rats with concomitant hypertension and hyperlipemia.
Acupunct Res. CAS Google Scholar. Farkas E, Luiten PGM, Bari F. Permanent, bilateral common carotid artery occlusion in the rat: A model for chronic cerebral hypoperfusion-related neurodegenerative diseases. Brain Res Rev. Jiang X, Niu X, Guo Q, Dong Y, Xu J, Yin N, et al.
FoxO1-mediated autophagy plays an important role in the neuroprotective effects of hydrogen in a rat model of vascular dementia. Kazuo K, Yoshiki Y, Tsutomu S, Shiro S, Emi OM, Takuma M, et al.
Chronic mild reduction of cerebral perfusion pressure induces ischemic tolerance in focal cerebral ischemia. Article Google Scholar. Ying CJ, Zhang F, Zhou XY, Hu XT, Chen J, Wen XR, et al. Anti-inflammatory effect of astaxanthin on the sickness behavior induced by diabetes mellitus.
Cell Mol Neurobiol. Zhang X-S, Zhang X, Wu Q, Li W, Zhang Q-R, Wang C-X, et al. Mar Drugs. Hussein G, Nakamura MQ, Iguchi T, Goto H, Sankawa U, Watanabe H.
Shen H, Kuo C-C, Chou J, Delvolve A, Jackson SN, Post J, et al. Astaxanthin reduces ischemic brain injury in adult rats. FASEB J. Lee D-H, Lee YJ, Kwon KH. Neuroprotective effects of astaxanthin in oxygen-glucose deprivation in SH-SY5Y cells and global cerebral ischemia in rat.
J Clin Biochem Nutr. Zhou X, Zhang F, Hu X, Chen J, Wen X, Sun Y, et al. Inhibition of inflammation by astaxanthin alleviates cognition deficits in diabetic mice. Physiol Behav. Tian X, Liu Y, Ren G, Yin L, Liang X, Geng T, et al. Resveratrol limits diabetes-associated cognitive decline in rats by preventing oxidative stress and inflammation and modulating hippocampal structural synaptic plasticity.
Deng W, Lu H, Teng J. Nootropics are supplements or compounds that enhance cognitive performance. They increase mental functions such as memory and attention.
Nootropics increase the blood circulation to the brain as well as boosting the energy and oxygen flow to the brain. Oxidative stress and free radicals damage nerve cells and decrease cognitive function. Therefore, the elimination of free radicals in the brain supports cognitive health.
As a potent antioxidant, natural astaxanthin plays an important role in the protection against oxidative damage. This is mediated by a variety of mechanisms, such as the elimination of singlet oxygen and radicals, the suppression of lipid peroxidation and the regulation of gene expression associated with oxidative stress.
The energy production process that takes place in the mitochondria generates huge amounts of free radicals and can cause a redox imbalance, which fosters mitochondrial dysfunction and, ultimately, leads to neurodegenerative conditions.
Natural astaxanthin works against lipid peroxidation in the mitochondria and is, in this respect, times more effective than vitamin E. The AstaReal Group is a pioneer in the cultivation and research of Haematococcus pluvialis , from which the valuable antioxidant is derived.
In the early s, AstaReal became the first company in the world to commercially produce natural astaxanthin from microalgae. Today, with a portfolio of more than 70 human clinical trials conducted among in excess of participants, AstaReal is the most studied brand of natural astaxanthin worldwide.
The majority of astaxanthin products on the market are derived from synthetic production. There is evidence that synthetic astaxanthin is significantly more inferior than astaxanthin from microalga with regard of anti-inflammatory and antioxidant properties.
Therefore, when choosing an astaxanthin supplier, companies should pay attention to production methods, the stability and purity of their products, the astaxanthin content in the biomass and their quality certifications. The pioneer cultivates and processes its algae indoors under controlled conditions in specially designed photobioreactors.
Health prevention and the desire for a better cognitive function are becoming increasingly important, with more and more people aware of the benefits of preventing diseases at a young age rather than having to treat them in later life.
Manufacturers can use this growing awareness and understanding to shape their products and communication … sand create premium dietary supplements containing value-added specialty ingredients.
Home Ingredients Boosting cognitive power with natural astaxanthin. A powerful and safe supplement Animals and humans cannot synthesise astaxanthin but must absorb it through food. The mitochondrion corollary The energy production process that takes place in the mitochondria generates huge amounts of free radicals and can cause a redox imbalance, which fosters mitochondrial dysfunction and, ultimately, leads to neurodegenerative conditions.
One step ahead Health prevention and the desire for a better cognitive function are becoming increasingly important, with more and more people aware of the benefits of preventing diseases at a young age rather than having to treat them in later life. References M. Katagiri, et al. Yook, et al. Natl Acad.
US A , — Nishida, et al. Nakagawa, et al. Capelli, D.
Astaxanthin Digestive system benefits, a carotenoid pigment found in various marine organisms, has Astaxanthon considerable attention Astaxanthin for focus and concentration to its potential impact on brain concenteation. This naturally cncentration compound has powerful antioxidant cnocentration that are crucial in protecting Astaxanthin for focus and concentration brain from oxidative stress. Oxidative stress is a phenomenon associated with an imbalance between free radicals and the body's ability to neutralize them. Over time, this imbalance can lead to cell damage, which can trigger a variety of diseases, including neurodegenerative disorders. Antioxidants like astaxanthin serve as an important line of defense against this imbalance. Astaxanthin has been identified as a potent antioxidant, even more powerful than other well-known antioxidants like beta-carotene and vitamin E.Astaxanthin for focus and concentration -
conducted a randomised, double-blind, placebo-controlled study involving 44 subjects over 12 weeks. Subjective user evaluation and the Cognitrax cognitive test were used to measure composite memory domain.
The reported results indicate that the astaxanthin-tocotrienols group showed a significant improvement in composite memory and verbal memory in Cognitrax at 12 weeks compared with the placebo group.
Additionally, the astaxanthin-tocotrienols group showed a significant improvement in subjective ability to recall memories, compared with the placebo group.
Lead author and part of BGG Japan Co, Takahiro Sekikawa, PhD, said further studies are needed in order to understand the reason for this synergistic benefit. Using a sample of 28 healthy, active, non-depressed adult subjects aged 26 to 63 years, researchers studied the effect of supplementation with AstaZine Natural Astaxanthin, compared to a placebo, over eight weeks.
Scientists observed significant improvements in three critical markers including feelings of depression, mental fatigue and overall mood state were found at the end of the study. Show more. Supporting the liver function will also help to keep the normal structure of the brain working in optimal condition.
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Behavioral and Brain Functions foor 16 Hunger control, Article number: 10 Ror this article. Metrics details. The purpose of this Anti-angiogenesis therapy for kidney cancer concentrationn to evaluate the effect of astaxanthin AST on cognition function, inflammatory response and oxidative stress in vascular dementia VD mice. VD mice model was established by left unilateral common carotid arteries occlusion LUCCAO. Following LUCCAO, AST was intragastrically administered for 30 days.
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