MPTP慢性帕金森病小鼠海马内氧化应激与细胞凋亡蛋白的表达

目的 观察 MPTP慢性帕金森病小鼠海马氧化应激指标及细胞凋亡相关蛋白的表达.方法 应用MPTP制备慢性帕金森病模型,观察行为学改变,Morris水迷宫实验,检测模型组和对照组小鼠海马内超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）及丙二醛（MDA）舍量变化,以及免疫组织化学方法、RT-PCR方法、Western blot方法检测海马Bax和Bel-2蛋白表达.结果 慢性帕金森病模型小鼠行为学特点为震颤、活动减少;水迷宫实验结果提示认知功能降低;与对照组海马比较：模型组海马SOD、GSH含量均下降,而MDA含量升高（P〈0.05）;模型组海马Bax蛋白表达增高,而Bel-2蛋白表达下降（P〈0.05）.结论 氧化应激在慢性帕全森病认知功能障碍发病机制中起重要作用,而Bax和Bcl-2蛋白参与了氧化应激诱导海马神经元凋亡的调控过程.

Oxidative Stress and Expression of Apoptosis Protein of Rat Hippocampal for MPTP-induced Parkinson's Disease

Objective To study the oxidative stress and apoptosis relative protein expression of the hippocampus in the MPTP-induced mouse model of parkinson＇s disease. Methods MPTP is injected into the mouse to produce chronic PD models. Activities of superoxide dismutase （SOD） ,contents of reduced glutathione（GSH） and malondialdehyde（MDA） in the injured and normal striatum are measured using assay kits; levels of Bax and Bcl-2 are detected by immunohistological staining, RT-PCR and Western blot in the hippocampus. Results The model mouse shows tremor, dyskinesia, and cognitive impairment ; compared with the control group, activities of SOD and contents of GSH in the cortex decrease significantly with contents of MDA increasing （P 〈 0. 05 ） ;levels of Bax increases with the expression of Bcl-2 decreasing. Conclusion Oxidative stress plays a key role in PD with cognitive impairment. Furthermore, Bax and Bcl-2 are involved in the regulation of apoptosis under oxidative stress induced by MPTP.