摘要
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（△ψm）及凋亡的影响。方法利用Rot诱导的分化PCI2细胞建立帕金森病rPD）细胞模型，应用不同浓度RFP（100、200、300μmol／L）预先干预，分别采用MTT法检测PCI2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2．5μmol／LRot可使PCI2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、300μmol／LRFP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PCI2细胞的损伤。且这种作用呈浓度依赖性。
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 of Parkinson＇ s disease in rat pheochromocytoma（PC 12） 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.
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2009年第9期907-910,共4页
Chinese Journal of Neuromedicine
关键词
利福平
鱼藤酮
活性氧
线粒体膜电位
帕金森病
Rifampicin
Rotenone
Reactive oxygen species
Mitochondrial transmembrance potential
Parkinson＇s disease
