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Effect of topiramate on apoptosis-related protein expression of hippocampus in model rats with Alzheimers disease

机译:托吡酯对阿尔茨海默病模型大鼠海马细胞凋亡相关蛋白表达的影响

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OBJECTIVES: Alzheimer’s disease is an age-related neurodegenerative disease and a synaptic function defect disease, the clinical symptoms are mainly progressive cognitive impairment, affecting patient’s social function. Aim of this report was to investigate the effect of topiramate on apoptosis-related protein expression (Bcl-2, Survivin, Fas, Bax and Caspase-3) in the hippocampus of a rat model with Alzheimers Disease (AD). MATERIALS AND METHODS: Thirty-six adult Wistar rats were randomly divided into a control group, a model group and a test group. A dose of amyloid beta-protein 1-40 (Aβ1-40) was injected into the hippocampus of the rats in the model and test groups, and the control rats are injected with same amount of saline. After AD model was successfully established, the rats in each group were administrated with an i.p. injection of topiramate (20 mg/kg/d) for 30 days. The effect of topiramate on the apoptosis-related protein levels in hippocampus neurons was studied by immunohistochemistry. RESULTS: The number of Bcl-2 and Survivin positive cells and optical density in hippocampus of rats in test group was more than those of rats in model groups, but less than those of rats in control group (p < 0.01); Fas, Bax and Caspase-3 positive cells and optical density in hippocampus of rats in test group was less than those of rats in the model group, but more than those of rats in control group (p < 0.01). CONCLUSIONS: Alzheimer’s disease can induce apoptosis of hippocampus neurons in rats. Topiramate can prevent apoptosis of hippocampus neurons, at least in part, by increasing expression of Bcl-2 and Survivin and decreasing expression of Fas, Bax and Caspase-3.
机译:目的:阿尔茨海默氏病是一种与年龄相关的神经退行性疾病和突触功能缺损疾病,临床症状主要是进行性认知障碍,影响患者的社会功能。本报告的目的是研究托吡酯对阿尔茨海默氏病(AD)大鼠模型海马中凋亡相关蛋白表达(Bcl-2,Survivin,Fas,Bax和Caspase-3)的影响。材料与方法:将36只成年Wistar大鼠随机分为对照组,模型组和试验组。在模型和试验组的大鼠海马中注射一定剂量的淀粉样蛋白1-40(Aβ1-40),并向对照组大鼠注射等量的生理盐水。成功建立AD模型后,对每组大鼠进行腹膜内注射。注射托吡酯(20 mg / kg / d)30天。通过免疫组织化学研究了托吡酯对海马神经元凋亡相关蛋白水平的影响。结果:试验组大鼠海马Bcl-2和Survivin阳性细胞数及光密度高于模型组,但低于对照组(p <0.01)。实验组大鼠海马Fas,Bax和Caspase-3阳性细胞及光密度低于模型组,但高于对照组(p <0.01)。结论:阿尔茨海默氏病可以诱导大鼠海马神经元凋亡。托吡酯可通过增加Bcl-2和Survivin的表达并降低Fas,Bax和Caspase-3的表达来至少部分地阻止海马神经元的凋亡。

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