利福平对鱼藤酮诱导的分化PC12细胞线粒体损伤的保护作用

目的 探讨利福平(RFP)对鱼藤酮(Rot)诱导的分化PC12细胞活性、胞内活性氧(ROS)水平、线粒体膜电位(AWm)及凋亡的影响. 方法 利用Rot诱导的分化PC12细胞建立帕金森病(PD)细胞模型,应用不同浓度RFP(100、200、300 μmol/L)预先干预,分别采用MTT法检测PC12细胞活性、流式细胞仪检测胞内ROS生成量、荧光显微镜和流式细胞仪检测△ψm及凋亡的变化.结果 2.5 μmol/L Rot可使PC12细胞活性降低.ROS生成、△ψm去极化程度和细胞凋亡率增加;100、200、300 μmol/L RFP预处理对上述变化有抑制作用,且浓度越大,作用越明显. 结论 RFP可能通过稳定△ψm、降低细胞内ROS生成来对抗Rot对分化PC12细胞的损伤,且这种作用呈浓度依赖性.

Rifampicin protects rotenone-induced mitochondrial damage in differentiated PC12 cells

Objective To explore the effects ofrifampicin(RFP)on the cell viability.reactive oxygen species(ROS)formation,the change of mitochondrial transmembrance potential(△ψm)and cell apoptosis induced by rotenone(Rot)in differentiated PC12 cells.Methods Rot was added to make a model ofParkinson's disease in rat pheochromocytoma(PCI2)cells in the presence of RFP.Cell viability was determined by MTT assay.Change of △ψm and cell apoptosis were measured by fluorescence microscope and flow cytometry respectively.Results Compared with control group and 300 μmol/L RFP group,cell viability was significantly decreased but depolarization of △ψm,ROS formation and cell apoptosis rate were significantly increased in 2.5 μmol/L Rot group.Compared with 2.5 μmol/L Rot group,RFP(100,200 and 300 μmol/L)pretreated groups,cell viability was significantly increased,but depolarization of △ψm、ROS formation and cell apoptosis rate were significantly decreased in a dose-dependent manner.Conclusion RFP may protect the damage induced by Rot in differentiated PC12 by reducing depolarization of △ψm and ROS formation in a dose-dependent manner.