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

An Experimental Study on the Mitochondrial Dysfunction of MES 23.5 Cell Induced by 1-Methyl-4-Phenylpyridium

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 MES2 3 .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 (△ Ψ m)和氧自由基 (ROS)的变化。结果 MES2 3 .5细胞活力在 MPP+组显著减低 ,且与浓度呈正相关 ,GSH+MPP+组轻度减低 ,而 MPTP组不降低。此外 ,用 MPP+ 处理后 MES 2 3 .5细胞线粒体 △ Ψ m明显下降和 ROS生成显著增加。结论 线粒体△ Ψ m下降及ROS生成增多可能参与了 MPP+ 诱导黑质

Objective To investigate the mitochondrial dysfunction mechanism of 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+.