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Excitotoxicity and oxidative stress are central to the pathology of the nervous system, and inhibition of excitotoxicity induced by glutamate is one of the therapeutic goals determined for stroke. The present study aimed to investigate the effects of Astaxanthin, a potent natural antioxidant, on complications caused by acute cerebral stroke. In this research, 60 male Wistar rats were used which were divided into 5 groups as follow: (1) the sham group (vehicle), (2) the ischemic control group (vehicle), and the ischemic groups treated by Astaxanthin with doses of 25, 45, and 65 mg/kg. In the ischemic groups, ischemic model was performed by middle cerebral artery occlusion (MCAO) method, and the Astaxanthin administration was carried out after the artery occlusion and before opening the artery. The obtained results indicated that Astaxanthin could significantly reduce stroke volume, neurological deficits, and lipid peroxidation. Moreover, it was able to restore total oxidant status (TOS) and caspase 3 level to the normal level. The activity of antioxidant enzyme glutathione peroxidase (GPX), and the expression of catalase, GPx and nuclear factor kappa B (NFκb) genes, which were reduced after ischemia, were increased. This phenomenon was particularly pronounced for glutamate transporter 1 (GLT-1). Furthermore, Astaxanthin decreased the augmented pro-apoptotic gene Bax and restored the reduced Bcl2 expression to the normal level. Significant effects on the P53 and PUMA expression were not observed. Overall, the medium dosage of Astaxanthin appears to be more effective in reducing the complications of ischemia, particularly on our major study endpoints (stroke volume and neurological defects). Longer studies with a more frequent administration of Astaxanthin are required to better understand the precise mechanism of Astaxanthin.
相似文献Objective
To study the putative effects of Advanced Oxidation Protein Products (AOPPs) and Advanced Glycation End Products (AGEs) in the development and progression of cardiovascular disease (CVD).Methodology
AGEs, AOPPs, e-NOS, lipid profile, circulating stress and inflammatory biomarkers were evaluated among fifty cardiovascular patients and fifty controls. Independent student’s t-test was done for statistical analysis.Results
The malondialdehyde mean level in CVD patients (5.45?nmol/ml) was significantly higher than control (1.36?nmol/ml) (p value?=?0.018). Nitric oxide in CVD patients (55.72?ng/ml) was remarkably increased as compared to normal subjects (19.19?ng/ml). A significant change in the mean serum level of AGEs in CVD patients (2.74?ng/ml) and normal individuals (0.85?ng/ml) was recorded (p value?=?0.000). The AOPPs also showed significant increased levels in CVD group (132.07?ng/ml) in comparison with normal subjects (83.05?ng/ml) (p value?=?0.011). The mean eNOS serum level in CVD group (15.50?U/L) was higher than control group (11.28?U/L) (p value?=?0.004). Cardiovascular disease patients, in comparison with healthy controls, showed increased level of total cholesterol (5.48?mmol/L vs 4.45?mmol/L), triglycerides (2.59?mmol/L vs 1.24?mmol/L), and low density lipoprotein (2.47?mmol/L vs 2.31?mmol/L) along with decrease in high density lipoprotein (1.39?mmol/L vs 1.74?mmol/L). The mean MMP-11 serum levels in CVD group (98.69?ng/ml) was almost double of control group (45.60?ng/ml) (p value?=?0.017). The mean serum level of TNF-α and IL1-α were 32.16?pg/ml and 6.64?pg/ml in CVD patient. The significant decreasing trend of SOD (p value?=?0.041), CAT (p value?=?0.018), GSH (p value?=?0.036) and GRx (p value?=?0.029) but increasing drift of GPx (0.023) level was observed in CVD patients.Conclusion
This study provides strong evidence that CVD patients presented with elevated oxidative stress, enhanced inflammation and lipid profile in their serum. Therefore, the study strongly approves that AGEs, AOPPs, inflammatory and lipoxidative biomarkers hold predictive potential in causing and aggravating the disease, thus by controlling these factors CVD progression can be inhibited. 相似文献Synbiotics are known to exert multiple beneficial effects, including anti-inflammatory and antioxidant actions. The aim of this study was to evaluate the effects of synbiotic supplementation on carotid intima-media thickness (CIMT), biomarkers of inflammation, and oxidative stress in people with overweight, diabetes, and coronary heart disease (CHD). This randomized, double-blind, placebo-controlled trial was conducted and involved 60 people with overweight, diabetes, and CHD, aged 50–85 years old. Participants were randomly allocated into two groups to take either synbiotic supplements containing three probiotic bacteria spices Lactobacillus acidophilus strain T16 (IBRC-M10785), Lactobacillus casei strain T2 (IBRC-M10783), and Bifidobacterium bifidum strain T1 (IBRC-M10771) (2 × 109 CFU/g each) plus 800 mg inulin or placebo (n = 30 each group) for 12 weeks. Fasting blood samples were taken at baseline and after the 12-week intervention period to determine metabolic variables. After the 12-week intervention, compared with the placebo, synbiotic supplementation significantly reduced serum high-sensitivity C-reactive protein (hs-CRP) (− 3101.7 ± 5109.1 vs. − 6.2 ± 3163.6 ng/mL, P = 0.02), plasma malondialdehyde (MDA) (− 0.6 ± 1.0 vs. − 0.1 ± 0.3 μmol/L, P = 0.01), and significantly increased nitric oxide (NO) levels (+ 7.8 ± 10.3 vs. − 3.6 ± 6.9 μmol/L, P < 0.001). We did not observe any significant changes of synbiotic supplementation on other biomarkers of oxidative stress and CIMT levels. Overall, synbiotic supplementation for 12 weeks among people with overweight, diabetes, and CHD had beneficial effects on serum hs-CRP, plasma NO, and MDA levels; however, it did not have any effect on other biomarkers of oxidative stress and CIMT levels.
相似文献