【摘要】 目的:探讨1-甲基-4-苯基-吡啶盐(MPP~+)作用下,还原型谷胱甘肽(GSH)对MES 23.5多巴胺神经元细胞氧化损伤的保护作用及其机制。方法:CCK8法检测MES 23.5细胞存活率,细胞分为5组:对照组、MPP~+组、MPP~++L-Dopa组、MPP~++GSH组、MPP~++L-Dopa+GSH组。流式细胞术检测凋亡率及线粒体膜电位;通过DCFH-DA探针检测ROS含量;用比色法,检测MDA水平、CAT活性。结果:GSH可以抑制MPP~+所致的MES 23.5细胞存活率、△ψm及CAT活性水平降低,凋亡率、ROS含量及MDA水平升高(P<0.05);GSH与L-Dopa合用,这种抑制作用更明显(P<0.05)。结论:GSH与L-Dopa合用对MPP~+诱导的MES 23.5细胞氧化损伤有明显保护作用,机制可能与抑制细胞线粒体损伤及脂质过氧化,发挥抗氧化作用有关。更多还原

【Abstract】 Objective: To investigate the neuroprotective role and mechanism of glutathione against 1-methyl-4-phenylpyridium( MPP~+)-induced neurotoxicity in MES 23. 5 cells. Methods: CCK8 method was used to detect the viability of MES 23. 5 cells. Control group,MPP~+group,MPP~++ L-Dopa group,MPP~++ GSH group and MPP~++ L-Dopa+ GSH group were included in the study. The apoptosis rate and mitochondrial membrane potential( △ψm) were measured by flow cytometry. The ROS levels,MDA content and CAT activity were determined by the DCFH-DA probe and colorimetric method. Results: For MPP~+-induced MES 23. 5 cells,the significant decrease of viability,△ψm and CAT were ameliorated by GSH which also caused the inhibition of increase of apoptosis rate,ROS levels and MDA content( P < 0. 05). This inhibition was more pronounced when GSH combined with L-Dopa( P < 0. 05). Conclusion:Glutathione combined with L-Dopa exerts neuroprotective effects against MPP~+-induced neurotoxicity in MES 23. 5 cells,and the mechanism might be related to the inhibition of mitochondrial damage and lipid peroxidation followed by antioxidant role of GSH.更多还原