α-突触核蛋白促进过氧化氢诱导的多巴胺能神经细胞凋亡

摘要

目的 研究α-突触核蛋白(α-synuclein,α-syn)在过氧化氢(hydrogen peroxide,H2O2)诱导的多巴胺能神经细胞凋亡中的作用.方法 通过瞬时转染重组质粒pEGFP-α-syn和pcDNA-α-syn到MES23.5多巴胺能神经细胞建立过表达α-syn细胞模型.细胞外添加H2O2 (200 μmol/L)处理细胞.Hoechst 33258荧光标记细胞核及AO/PI(吖啶橙/碘化丙啶)双染检测细胞凋亡.Mitotracker线粒体探针标记线粒体.结果 H2O2可增加α-syn向线粒体和细胞核的转运；H2O2可单独引起细胞凋亡,但过表达α-syn细胞的凋亡率显著高于空载质粒转染细胞(P＜0.05).结论 α-Syn增强了H2O2诱导的多巴胺能神经细胞凋亡.%Objective To investigate the role of a-synuclein ( a-syn) in hydrogen peroxide (H2 02) -induced apoptosis of dopaminergic neuronal cells. Methods a-Syn overexpression cell model was established by transient transfection of plasmids pEGFP-a-syn or pcDNA-a-syn into MES23.5 dopaminergic neuronal cells. The cells were treated with H2O2 (200 u.mol/L) to induce cell apoptosis. Hoechst 33258 and AO/PI fluorescent labeling were used to examine apoptosis. Mitochondrial probe Mitotracker was used to label mitochondria. Results H2 02 increased translocation of a-syn into mitochondria and nuclei and induced apoptosis of both the vector control cells and a-syn overexpression cells. More apoptotic cells were found in a-syn overexpression cells than in vector control cells ( P < 0. 05 ). Conclusion a-Syn enhances H2O2-induced apoptosis of dopaminergic neuronal cells.