scholarly journals Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yunxia Dong ◽  
Wei Hong ◽  
Zhiyin Tang ◽  
Yan Gao ◽  
Xiuying Wu ◽  
...  
Keyword(s):  
Normal Saline ◽  
Water Maze ◽  
Escape Latency ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Sprague Dawley ◽  
Sevoflurane Group ◽  
Maze Test ◽  
Sprague Dawley Rats ◽  
Rhoa Signaling

To investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevoflurane group were injected with normal saline and inhaled with 3% sevoflurane for 2 h in three consecutive day; rats in the dexmedetomidine group were inhaled with 3% sevoflurane after intraperitoneal injection of dexmedetomidine 25 μg/kg. WB results showed that mBDNF, pTrkB/TrkB, and CREB were significantly decreased in the hippocampus of the sevoflurane group, which are significantly upregulated in the dexmedetomidine group. In the sevoflurane group, proBDNF, P75NRT, and RhoA were significantly increased, which were significantly lower than those in the dexmedetomidine group than those in the sevoflurane group. The expression BDNF was downregulated in the sevoflurane group, while the proBDNF was upregulated in the sevoflurane group. In the Morris water maze test, the escape latency of the sevoflurane group was significantly prolonged. In sevoflurane groups, the number of crossing platform was significantly reduced, the synaptic protein decreased significantly, and this effect was reversed in rats of the dexmedetomidine group. Dexmedetomidine could reduce synaptic plasticity decline in developing rats induced by sevoflurane, through downregulating the proBDNF-p75NTR-RhoA pathway and upregulating BDNF-TrkB-CREB.

scholarly journals Thymoquinone enhances sperm DNA integrity in nicotineinduced infertile male rats

2021 ◽  
Vol 18 (6) ◽  
pp. 1219-1225
Author(s):  
Farah Dayana Rosli ◽  
Noor Hashida Hashim ◽  
Yusmin Mohd Yusuf ◽  
Khairul Osman ◽  
Siti Fatimah Ibrahim ◽  
...  
Keyword(s):  
Normal Saline ◽  
Quantitative Polymerase Chain Reaction ◽  
Male Rats ◽  
Control Group ◽  
Dna Integrity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sperm Dna ◽  
Potential Benefits

Purpose: To assess the effects of thymoquinone (TQ) on the integrity of sperm DNA in nicotineinduced sperm impairment in rats. Methods: Adult male Sprague Dawley rats were randomized into four equal groups: control group received normal saline orally for 60 days; nicotine group was subcutaneously injected with 5 mg/kg/day nicotine for 30 days and then given normal saline for the next 30 days; TQ group was given normal saline for 30 days followed by TQ at 5 mg/kg/day for 30 days; and nicotine-TQ group received 5 mg/kg of nicotine for 30 days and 5mg/kg of TQ for another 30 days. Sperm DNA breakages were evaluated using Comet assay. The expression levels of protamine 1 (PT1) and transition nuclear protein 2 (Tnp2) genes which are essential for the proper compaction of the sperm DNA were analyzed by quantitative polymerase chain reaction (qPCR). Results: Thymoquinone significantly decreased DNA fragmentation in the sperm of nicotine-treated rats. However, there was no change in PT1 gene expression. Tnp2 was downregulated in the nicotine group and slightly upregulated in nicotine-TQ group (p < 0.05). Conclusion: The results demonstrate the potential benefits of TQ in improving sperm DNA quality of nicotine-induced male infertility.

scholarly journals THE NEPHROTOXICITY OF CONCURRENT USE OF ENALAPRIL AND GENTAMICIN IN RATS

2018 ◽  
Vol 11 (9) ◽  
pp. 348
Author(s):  
Imad M Al-ani ◽  
Khaleed R Algantri ◽  
Emad M Nafie ◽  
Sinan Mohammed Abdullah Al-mahmood
Keyword(s):  
Experimental Study ◽  
Serum Creatinine ◽  
Blood Urea Nitrogen ◽  
Normal Saline ◽  
Control Group ◽  
Sprague Dawley ◽  
Concurrent Administration ◽  
Urea Nitrogen ◽  
Concurrent Use ◽  
Sprague Dawley Rats

Objective: The present study was aimed to assess the concurrent administration of Enalapril (ENAL) and Gentamicin (GM) in the kidney of rats.Methods: Sixty male Sprague Dawley rats were divided into 4 main groups (n=15) according to the administered dose. Each main group was further subdivided into three subgroups according to the day of sacrificing (n=5). Group (C) was administered daily with normal saline as control, Group (E) was treated with oral ENAL (2 mg/kg/day), Group (G) was treated with GM (75 mg/kg/day), and Group (EG) was treated ENAL (2 mg/kg/day) and GM (75 mg/kg/day). The handling of the experiment persisted daily for 15 days, and the investigational examination carried out on days 5, 10, and 15.Results: The result showed that GM nephrotoxicity augmented with the period of the experimental study, there was rising in the levels of serum creatinine and blood urea nitrogen on the 10th day and persisted in rising significantly during the period on the 15th day of the experiment. Administration of ENAL showed no significant alteration from those of controls. While the concurrent administration of ENAL and GM showed that ENAL gradually increased GM nephrotoxicity, these physiological retrogressions were accompanied with intensive renal histopathological deteriorations.Conclusion: The present study has revealed that the concurrent administration of ENAL enormously aggravated the functional and histological nephrotoxicity of GM in rats.

scholarly journals Effect of Evodia rutaecarpa (Juss) Benth extract on Alzheimer disease in mice

2020 ◽  
Vol 19 (4) ◽  
pp. 823-828
Author(s):  
Ang Cai ◽  
Liu Xiao ◽  
Yan-Ping Zhou ◽  
Zhi-Guo Zhang ◽  
Quan-Wei Yang
Keyword(s):  
Cognitive Function ◽  
Alzheimer Disease ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Evodia Rutaecarpa ◽  
Mouse Hippocampus

Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in the animals treated with 400 mg/kg ERBE (20.5 ± 1.3 s) was significantly higher than untreated 3xTg-AD mice (12.4 ± 1.3 s, p < 0.01). In addition, ERBE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.4 ± 0.2, p < 0.05) and TrkB (1.1 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: The results suggest that ERBE administration may be a useful strategy for treating memory impairment induced by several neurodegenerative diseases. Keywords: Evodia rutaecarpa, Alzheimer, Memory impairment, NeuN-positive cells

Acupuncture Improves Cognitive Deficits and Increases Neuron Density of the Hippocampus in Middle-Aged Samp8 Mice

2012 ◽  
Vol 30 (4) ◽  
pp. 339-345 ◽  
Author(s):  
Guomin Li ◽  
Xuezhu Zhang ◽  
Haiyan Cheng ◽  
Xuemei Shang ◽  
Hui Xie ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Morris Water Maze ◽  
Cognitive Deficits ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Neuron Loss ◽  
Neuron Density ◽  
Maze Test ◽  
Samp8 Mice

Objectives To examine whether acupuncture could improve cognitive deficits and reduce the loss of neurons in mice models of ageing. Methods Male 7.5-month-old senescence-accelerated mouse prone 8 (SAMP8) and age-matched senescence-resistant inbred strains 1 (SAMR1) were divided into four groups (n=15 per group): SAMP8 acupuncture group (Pa), SAMP8 non-acupuncture point control group (Pn), SAMP8 control group (Pc) and SAMR1 normal control group (Rc). The behaviours were examined by the Morris water maze test and the neuron density in the hippocampus was estimated by the optical fractionator technique. Results The Morris water maze test demonstrated that the cognitive deficits of SAMP8 mice were improved by acupuncture treatment. Neuronal loss was found in hippocampal regions CA1 (−24%), CA3 (−18%) and DG (−28%) of Pc compared with Rc. The neuron number in hippocampal CA3 and DG of the Pa group was significantly increased by therapeutic acupuncture compared with the Pc group. Conclusions Acupuncture improved the cognitive impairment of middle-aged SAMP8 mice which could be attributed to the reduced neuron loss in hippocampal regions CA3 and DG. These results suggest that reducing neuron loss in the hippocampus by acupuncture is a potential therapeutic approach for the treatment of Alzheimer's disease and cognitive impairment diseases.

scholarly journals Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice

2021 ◽  
Vol 18 (9) ◽  
pp. 1903-1907
Author(s):  
Cen Su ◽  
Ping Niu ◽  
Yao-ming Xu ◽  
Ye Feng ◽  
Hai-ping Xia
Keyword(s):  
Cognitive Function ◽  
Protective Effect ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Immunohistochemical Assay ◽  
Maze Test ◽  
Acorus Tatarinowii

Purpose: To investigate the protective effect of Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice. Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in animals treated with 600 mg/kg ATE (24.8 ± 1.3 s) was significantly increased relative to ontreated 3xTg-AD mice (8.5 ± 1.0 s, p < 0.01). In addition, ATE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF (1.9 ± 0.4, p < 0.05) and TrkB (1.9 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: These results suggest that ATE treatment may be a useful strategy for managing memory impairment induced by several neurodegenerative diseases.

scholarly journals Dimethyl fumarate prevents acute lung injury related cognitive impairment potentially via reducing inflammation

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Xiaowei Wang ◽  
Yanbo Wang ◽  
Haiyan Pan ◽  
Ci Yan
Keyword(s):  
Cognitive Impairment ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Water Maze ◽  
Dimethyl Fumarate ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Maze Test ◽  
Evans Blue Extravasation ◽  
Brain Tissues

Abstract Objective Dimethyl fumarate (DMF) has been reported to exert a protective role against diverse lung diseases and cognitive impairment-related diseases. Thus this study aimed to investigate its role on acute lung injury (ALI) and related cognitive impairment in animal model. Methods C57BL/6 mice were divided into four groups: control group, DMF group, ALI group, and ALI + DMF group. For ALI group, the ALI mice model was created by airway injection of LPS (50 μL, 1 μg/μL); for ALI + DMF group, DMF (dissolved in 0.08% methylcellulose) was treated twice a day for 2 days, and on the third day, mice were injected with LPS for ALI modeling. Mice pre-administered with methylcellulose or DMF without LPS injection (PBS instead) were used as the control group and DMF group, respectively. Morris water maze test was performed before any treatment (0 h) and 6 h after LPS-induction (54 h) to evaluate the cognitive impairment of mice. Next, the brain edema and blood brain barrier (BBB) permeability of ALI mice were assessed by brain water content, Evans blue extravasation and FITC-Dextran uptake assays. In addition, the effect of DMF on the numbers of total cells and neutrophils, protein content in BALF were quantified; the inflammatory factors in BALF, serum, and brain tissues were examined by ELISA, qRT-PCR, and Western blot assays. The effect of DMF on the cognitive impairment-related factor HIF-1α level in lung and brain tissues was also examined by Western blot. Results DMF reduced the numbers of total cells, neutrophils and protein content in BALF of ALI mice, inhibited the levels of IL-6, TNF-α and IL-1β in BALF, serum and brain tissues of ALI mice. The protein expressions of p-NF-κB/NF-κB and p-IKBα/IKBα was also suppressed by DMF in ALI mice. Morris water maze test showed that DMF alleviated the cognitive impairment in ALI mice by reducing the escape latency and path length. Moreover, DMF lessened the BBB permeability by decreasing cerebral water content, Evans blue extravasation and FITC-Dextran uptake in ALI mice. The HIF-1α levels in lung and brain tissues of ALI mice were also lessened by DMF. Conclusion In conclusion, DME had the ability to alleviate the lung injury and cerebral cognitive impairment in ALI model mice. This protective effect partly associated with the suppression of inflammation by DMF.

scholarly journals Electroacupuncture Synergistically Inhibits Proinflammatory Cytokine Production and Improves Cognitive Function in Rats with Cognitive Impairment due to Hepatic Encephalopathy through p38MAPK/STAT3 and TLR4/NF-κB Signaling Pathways

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Jiling Huang ◽  
Zhigang Gong ◽  
Yingnan Kong ◽  
Yanwen Huang ◽  
Hui Wang ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Brain Tissue ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Model Group ◽  
Maze Test ◽  
Tnf Α ◽  
Serum Ammonia ◽  
The Brain

Objective. To investigate the effect of electroacupuncture (EA) on cognitive dysfunction in rats with hepatic encephalopathy and its underlying mechanism. Methods. Fifty Wistar rats were randomly divided into a normal group (n = 10) and model group (n = 40). Rat models of hepatic encephalopathy were established by administration of carbon tetrachloride and thioacetamide for a total of 12 weeks. At the 9th week after modeling, rats with cognitive impairment in the model group were identified by conducting the Morris water maze test, which were then randomly divided into a control group (CCl4) and treatment groups including EA group (CCl4 + EA), lactulose group (CCl4 + Lac), and EA plus lactulose group (CCl4 + CM), with 9 rats in each group. At the end of the 9th week, rats in CCl4 + Lac and CCl4 + CM groups had lactulose gavage at a dose of 10 mL/kg body weight, while normal control and CCl4 groups had gavage with the same volume of normal saline once a day for 21 days until the end of the experiment. Rats in CCl4 + EA and CCl4 + CM groups underwent acupuncture at Baihui (GV[DU]20), Shenting (GV[DU]24), and Zusanli (ST36) acupoints, among which EA at Baihui and Shenting acupoints were given once daily for 30 min lasting for 21 consecutive days. The effect of the treatment was measured by the Morris water maze test for learning and memory ability and magnetic resonance spectroscopy (MRS) for neuronal metabolism in the hippocampus of rats with hepatic encephalopathy. Pathological change in the rat hippocampus was observed by HE staining, while serum ammonia and liver function markers were detected. Western blot and real-time fluorescent quantitative PCR were used to detect the expressions of specific genes and proteins in the brain tissue. Results. Compared with those in the control group, rats undergoing EA had significantly shortened escape latency and increased number of platform crossing. H&E staining confirmed that EA improved brain tissue necrosis and ameliorated nuclear pyknosis in rats with hepatic encephalopathy. Significantly decreased levels of serum ammonia, alanine aminotransferase (ALT), aspartate transaminase (AST), total bilirubin (TBil), and total bile acid (TBA) were observed in rats undergoing EA, as well as improved levels of total protein (TP) and albumin (ALB). In addition, EA inhibited the brain expressions of TNF-α, IL-1β, IL-6, iNOS, TLR4, MyD88, NF-κB, p38MAPK, phosphorylated (p)-p38MAPK, STAT3, and p-STAT3 genes, as well as protein expressions of TNF-α, IL-6, TLR4, MyD88, NF-κB, p38MAPK, p-p38MAPK, STAT3, and p-STAT3. MRS showed increased Glx/Cr and decreased NAA/Cr, Cho/Cr and mI/Cr in the control group, and EA significantly reversed such changes in Glx/Cr and mI/Cr values. Conclusion. EA ameliorated the production of excessive proinflammatory cytokines in the hippocampus of rats with cognitive dysfunction secondary to hepatic encephalopathy, which also gave rise to subsequent changes such as reduced blood ammonia level, brain-protective activated astrocytes, and lower degree of brain tissue injury. The p38MAPK/STAT3 and TLR4/MyD88/NF-κB signaling pathways may be involved. EA can also improve the metabolism of NAA and Cho in the rat hippocampus and thereby improve learning and memory abilities.

scholarly journals Impact of amitriptyline on learning and memory

2021 ◽  
Vol 5 (1) ◽  
pp. 009-015
Author(s):  
CC Mfem ◽  
SA Seriki
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Acquisition Trial ◽  
Water Maze ◽  
Treated Group ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Maze Test ◽  
Significant Difference ◽  
Retention Trial

Background/aim: Amitriptyline belongs to class of known as tricycline antidepresant (TCA) that is being used to treat anxiety and depressive states. It may help improve mood and feelings of well-being, relieve anxiety and tension, help to improve sleep and increase energy level. The study investigated the effect of amitriptyline on learning and memory using eighteen (18) healthy Swiss mice of both sexes weighing 16 – 25 g. Method: The animals were divided into three (3) groups consisting of six (6) animals each. Group 1 served as the control group, Group 2 was administered with amitriptyline at a dose of 3 mg/kg body weight dissolved in 3 mls of distilled water, and used to test for learning, while Group three was also given similar administration like Group 2, but used to test for memory. All the animals were tested for learning and memory performance using Novel object recognition task and Morris water maze test. Results: The results obtained from the Novel object recognition task showed that there was a significant decrease (p < 0.05) in total object approach in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant decrease (p < 0.05) in retention trial of amitriptyline group when compared to retention trial in the control group. There was a significant decrease (p < 0.05) in total duration exploring objects in acquisition trial of amitriptyline treated group when compared to the acquisition trial of the control group. There was a significant increase (p < 0.05) in total duration exploring objects in retention trial of amitriptyline treated group when compared to the retention trial of the control group. There was a significant decrease (p < 0.05) in the index of habituation of amitriptyline treated group when compared to the control group. The index of discrimination showed a significant increase (p < 0.05) in amitriptyline treated group when compared to the control group and a significant decrease (p < 0.05) in amitriptyline group when compared to the control group. In the Morris water maze test, Day 1 – 3 were for acquisition training, day 4 – 6 reversal training, day 7 the probe trial day and day 8 the visible platform day. During acquisition training in the Morris water maze test, there was no significant difference in Swim latencies in day 1 and 2. However in day 3, there was a significant increase (p < 0.05) in swim latency of group compared to control group and a significant decrease (p < 0.05) in swim latency of amitriptyline treated group compared to the control group. During reversal training in day 1, 2 and 3, there was no significant difference in swim latency among the three groups. Results for the retention quadrant in the probe trials showed a significant decrease (p < 0.01) in amitriptyline group when compared to the control group. Conclusion: Results suggest that amitriptyline impairs learning and memory functions.

scholarly journals EVALUATION OF MEMORY-ENHANCING ACTIVITY FOR ERYTHRININE FROM LEAF EXTRACT OF ERYTHRINA INDICA

2019 ◽  
pp. 101-103
Author(s):  
KAMALRAJ R ◽  
SUBHASHREE G R
Keyword(s):  
Normal Saline ◽  
Water Maze ◽  
Leaf Extract ◽  
Positive Control ◽  
Negative Control ◽  
Test Method ◽  
Morris Water Maze Test ◽  
Memory Enhancement ◽  
Maze Test ◽  
Memory Enhancing

Objective: The objective of the study was to investigate the memory-enhancing activity for erythrinine (ring-c-oxygenated Erythrina alkaloid) from leaf extract of Erythrina indica in mice. Methods: The study protocol designed in the way that it was carried out for 21 successive days by administrating the 5 mg/kg, s.c doses of isolated erythrinine to mice and the profile was challenged against the mice feeds with normal saline as a positive control and the mice treated with 5 mg/kg, s.c corticosterone as a negative control for the amnesia using Morris water maze test method. Results: Erythrinine-administered mice are showing remarkable retention of the memory (9.07±0.52) on the 21st day as such of the positive control normal saline (10.14±0.22) and against the negative control corticosterone-injected mice (70.86±0.54). Conclusions: The dose of 5 mg/kg s.c of isolated erythrinine from the leaf of E. indica shows the remarkable memory enhancement when it was investigated with the memory weakening induced test by corticosterone in mice’s using 5 mg/kg s.c. However, further studies required to elucidate the exact mechanism of action for developing its as potent memory-enhancing drug.

Improvement of Impaired Memory in Mice by Schisandrin

2013 ◽  
Vol 750-752 ◽  
pp. 1533-1538
Author(s):  
Yan Chun Wang ◽  
Kuang Ren ◽  
Nan Shen ◽  
Xiao Dong Huang ◽  
Hong Yan Fan
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Cellular Response ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Tissue Samples ◽  
Pentobarbital Sodium ◽  
Maze Test

We assessed the effectiveness and mechanism of action of schisandrin on modulation of learning and memory disorders in mice. Memory impairment was established in mice by intraperitoneal injection of pentobarbital sodium (20 mg/kg). Schisandrin (0.5, 1.0, 2.0g/kg) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of schisandrin to reduce phenobarbital-induced learning and memory impairment. The levels of superoxide dismutase (SOD) nitric oxide (NO) and catalase (CAT) were measured in brain tissue samples taken from the mice. Other biomarkers measured included expression of nuclear transcription factor-kappa-B (NF-κB) and brain-derived neurotrophic factor (BDNF) in the hippocampus CA1 region, which were determined by immunohistochemical analysis. On the fifth day of treatment, the mice in the pentobarbital sodium group performed worse on the Morris water maze test compared to untreated controls (P<0.01), which could be prolonged after schisandrin treatment (P<0.05 for="" low="" and="" intermediate="" dose="" groups="" analysis="" of="" brain="" tissues="" showed="" that="" compared="" with="" the="" control="" group="" no="" levels="" were="" increased="" sod="" cat="" activity="" decreased="" in="" pentobarbital="" sodium="" i="">P<0.01). After treatment with schisandrin, the NO levels were significantly decreased (P<0.01), while SOD and CAT activity increased (P<0.01). Immunohistochemistry analysis showed that, in phenobarbital only group, the protein expression of BDNF decreased, NF-κB increased compared to untreated controls, and schisandrin could reverse this trend (P<0.05 and="" i="">P<0.01, respectively). The results suggest that schisandrin is effective in improving the learning and memory deficiency induced by pentobarbital sodium, the mechanism of which may be related modulation of cellular response to oxidative stress.

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