1-甲基-4-苯基吡啶离子诱导MES 23.5细胞线粒体功能异
常的实验研究
杨秀丽;陈生弟;刘振国;乐卫东
【期刊名称】《中国神经免疫学和神经病学杂志》 【年(卷),期】2001(008)002
【摘要】Objective To investigate the mitochondrial dysfunction mechanismof dopaminergic neuron death induced by 1-methyl-4-phenylpyridium（MPP+）. Methods After the incubation of MES 23.5 cells with different concentration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP), MPP+ and MPP+ plus glutathion (GSH), the membrane potential (△Ψm) and reactive oxygen species (ROS) of mitochondria were tested by MTT assay and flow cytometry (FCM). Results The MES 23.5 cells viability was decreased in MPP+, but not in MPTP, and slightly reduced in MPP+ plus GSH. Furthermore, decreased △Ψm and increased ROS production in MES 23.5 cells mitochondria were found significantly with MPP+-treatment.Conclusions The reduced △Ψm and elevated ROS production in MES 23.5 cells mitochondria may be involved in the mechanism of the dopaminergic neuron death induced by MPP+.%目的 探讨1-甲基-4-苯基吡啶离子（MPP+）诱导多巴胺（DA）能神经元死亡的线粒体功能异常机制。方法 不同浓度的1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)、MPP+及还原型谷胱甘肽(GSH)与MES23.5细胞共同培养，采用MTT比色法及流式细胞术检测细胞线粒体膜电势（△Ψm）
1-甲基-4-苯基吡啶离子诱导MES 23.5细胞线粒体功能异常的实验研究
