人参皂苷Re对慢性缺血致血管痴呆大鼠的线粒体保护作用

发布时间：2018-04-07 15:27

本文选题：血管性痴呆　切入点：线粒体　出处：《吉林大学》2017年硕士论文

【摘要】：目的:探讨人参皂苷Re对慢性缺血性血管痴呆(VD)大鼠海马神经元缺血损伤和线粒体功能障碍的保护作用,为开发安全有效的防治VD药物提供实验依据。方法:应用分次离断结扎双侧颈总动脉法建立VD大鼠模型;利用Morris水迷宫和HE染色判定模型构建效果;采用试剂盒提取各组线粒体及蛋白质,并通过电镜技术、Western-blot实验和H_2O_2试剂盒比较各组差异。利用真空泵和CO_2孵箱建立缺氧复氧模型,采用LDH释放量检测、DNA琼脂糖电泳及细胞形态观察验证模型建立效果。进一步通过检测各组LDH释放量、DNA断裂程度及细胞状态,并通过提取线粒体和蛋白质和应用Western Blot和H_2O_2试剂盒研究人参皂苷Re的作用。结果:分次离断结扎大鼠双侧颈总动脉后,大鼠认知能力下降,逃避潜伏期明显延长。细胞形态结构显示,大鼠海马神经元排列紊乱,细胞周围呈空泡化,失去正常结构。COX IV、PDH-A1和H_2O_2的表达结果显示,不同浓度的人参皂苷Re对大鼠VD线粒体的COX IV和PDH-A1的表达均有明显促进作用,而对H_2O_2释放量有一定抑制作用,表明人参皂苷Re可修复海马神经元的线粒体损伤。大鼠海马神经元经缺氧复氧后,其模型组LDH释放量增高、DNA断裂加剧、神经元突起退化及胞体固缩;而人参皂苷Re可有效抑制LDH释放、DNA断裂及突触退化,促进对线粒体COX IV和PDH-A1的表达,抑制H_2O_2的释放。结论:人参皂苷Re可对脑缺血所造成的海马神经元线粒体损伤起保护作用。人参皂苷Re可通过改善海马神经元的线粒体损伤,改善大鼠的认知能力。
[Abstract]:Objective: to investigate the protective effect of ginsenoside re on hippocampal neuronal ischemia injury and mitochondrial dysfunction in rats with chronic ischemic vascular dementia (VD), and to provide experimental evidence for the development of safe and effective drugs for the prevention and treatment of VD.Methods: VD rat model was established by severing and ligating bilateral common carotid artery, Morris water maze and HE staining were used to determine the effect of model construction, mitochondria and protein were extracted from each group by kit.Western blot and H_2O_2 kit were used to compare the differences.The model of anoxia and reoxygenation was established by vacuum pump and CO_2 incubator. The effect of the model was verified by using LDH release quantity to detect agarose electrophoresis and observe cell morphology.The effect of ginsenoside re on the activity of ginsenoside re was studied by detecting the amount of LDH released in each group and the cell state, and by extracting mitochondria and proteins, and using Western Blot and H_2O_2 kit to study the effect of ginsenoside re.Results: the cognitive ability of bilateral common carotid artery was decreased and the escape latency was prolonged.The morphological structure of the cells showed that the hippocampal neurons in the rats were disordered and vacuolated around the cells, and the expression of PDH-A1 and H_2O_2 were found to be lost in the normal structure.Different concentrations of ginsenoside re could obviously promote the expression of COX IV and PDH-A1 in VD mitochondria, but inhibit the release of H_2O_2, suggesting that ginsenoside re could repair the mitochondrial damage of hippocampal neurons.After hypoxia and reoxygenation, the release of LDH in the model group increased, the neurite degeneration and cell body pyknosis were aggravated, while ginsenoside re could effectively inhibit the LDH release and synaptic degeneration.Promote the expression of mitochondrial COX IV and PDH-A1 and inhibit the release of H_2O_2.Conclusion: ginsenoside re can protect hippocampal neuron mitochondria from cerebral ischemia.Ginsenoside re can improve the cognitive ability of rats by improving mitochondria damage of hippocampal neurons.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R285.5

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