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目的 :探讨caspase 3在 1 甲基 4 苯基吡啶离子 (1 methyl 4 phenylpyridinium ,MPP+ )诱发多巴胺能神经元凋亡中的表达。方法 :建立MPP+ 诱发中脑神经细胞凋亡模型 ,通过免疫组织化学染色及RT PCR检测方法 ,检测原代培养的 16d胎鼠的中脑多巴胺能神经元中caspase 3的表达。 结果 :在正常组和细胞凋亡组 (MPP+ 组 )的caspase 3在蛋白质和基因水平均有表达 ,但在细胞凋亡组中表达强度明显高于正常对照组 ,二者差异具有显著性。caspase 3的蛋白酶抑制剂Ac DEVD CHO可降低caspase 3的表达。 结论 :caspase 3参与MPP+ 诱发的多巴胺能神经元的凋亡过程 ,并起关键作用 ,以MPP+ 为诱导剂建立的中脑神经细胞凋亡模型可用于研究与帕金森病 (Parkin sondisease,PD)有关的细胞凋亡的调控机制和筛选抗PD药物
AIM: To investigate the expression of caspase 3 in 1-methyl-4-phenylpyridinium (MPP +) -induced dopaminergic neuron apoptosis. Methods: The apoptosis model of midbrain nerve cells induced by MPP + was established. The expression of caspase 3 in midbrain dopaminergic neurons was detected by immunohistochemical staining and RT PCR. Results: The expression of caspase 3 in both normal and apoptotic groups (MPP + group) was both at the protein and gene level, but significantly higher in the apoptotic group than in the normal control group. The difference was significant. Ac DEVD CHO, a protease inhibitor of caspase 3, decreases caspase 3 expression. CONCLUSIONS: Caspase 3 is involved in the apoptotic process of dopaminergic neurons induced by MPP + and plays a key role. The apoptosis model of mesencephalic neurons established by MPP + may be used to study the relationship between Parkinson’s disease and Parkinson’s disease The regulatory mechanism of apoptosis and screening anti-PD drugs