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机构地区:[1]安徽中医药大学 [2]省部共建新安医学教育部重点实验室,安徽合肥230038
出 处:《安徽医药》2015年第2期239-241,共3页Anhui Medical and Pharmaceutical Journal
摘 要:目的研究伊拉地平(ISR)对1-甲基-4-苯基吡啶离子(MPP+)损伤的PC12细胞的保护作用及可能机制。方法MPP+处理PC12细胞建立帕金森病细胞模型;4-甲基偶氮唑蓝(MTT)比色法检测细胞存活率;双氯荧光黄乙酸乙酯(DCFHDA)染色流式细胞术检测细胞内活性氧(ROS)的生成;JC-1染色流式细胞术检测细胞线粒体膜电位(MMP)。结果 1 mmol·L-1MPP+处理PC12细胞24 h后能明显抑制细胞生长(P<0.01);降低线粒体膜电位;ROS含量增加。2μmol·L-1伊拉地平预处理后,PC12细胞存活率显著增加(P<0.01);线粒体膜电位升高;ROS生成减少。结论伊拉地平对MPP+损伤的PC12细胞具有保护作用,其作用机制可能与维持线粒体正常膜电位,稳定线粒体功能,阻止线粒体氧化应激发生有关。Objective To stuty the protective effects of isradipine(ISR) against MPP+-induced injury in PC12 cells.Methods Rat pheochromocytoma(PC12) cells treated with MPP+were used as the cell model of Parkinson’s disease.The cell viability was detected by MTT assay.The mitochondrial transmembrane potential and the cellular ROS level were observed by spectrofluorometry.Results Compared with control group,the cell viability of PC12 cells treated with MPP+1 mmol&· L -1 for 24 h was significantly declined,ROS markedly generated and mitochondrial membrane potential was increased.Pretreatment with 2 μmmol&· L -1 isradipine increased the cell viability and the MMP,and reduced MPP+-induced intracellular ROS production.Conclusion Isradipine could protect against the MPP+-induced injury,whose protective mechanisms may be related to the maintenance of normal mitochondrial membrane poten-tial,stabilization of mitochondrial function and prevention of mitochondrial oxidative stress.
关 键 词:MPP+ PC12细胞 伊拉地平 氧化应激 帕金森病
分 类 号:R742.5[医药卫生—神经病学与精神病学]
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