摘要
目的:探讨鱼藤酮对多巴胺能细胞的毒性作用及其机制。方法:PC12细胞分为对照组和鱼藤酮组(Ro10 nM、Ro100 nM、Ro1μM组),分别用DMSO和10 nmol/L、100 nmol/L、1μmol/L鱼藤酮处理24 h,用噻唑蓝比色法检测细胞活性,流式细胞术检测细胞凋亡率、细胞线粒体膜电位,荧光底物酶活性法检测Caspase 3活性。结果:与对照组相比,Ro10 nM、Ro100 nM、Ro1μM组的细胞活力和细胞凋亡率呈剂量依赖性下降(P<0.05),其中Ro1μM组MTT吸光度为对照组的42.1%,凋亡率为41.9%。与对照组相比,各鱼藤酮组线粒体膜电位均下降及Caspase 3活性增高(P<0.05),其变化程度亦呈药物剂量依赖性。结论:鱼藤酮处理可诱导多巴胺能细胞凋亡,而且其凋亡程度具有剂量依赖性。
Objective： The neurotoxicity of rotenone in dopaminergic cells and the underlying mechanisms have been investigated.Methods： PC12 cells were treated with rotenone at different concentrations for 24 hours.MTT assay was used to evaluate the cell viability.Apoptosis was determined by apoptotic cell counting with flow cytometry after Annexin V-FITC staining.Mitochondrial membrane potentials were determined by flow cytometry technique.Caspase 3 activity was measured by fluorescence assay using the probe Ac-DEVD-AMC.Results： Rotenone induced a dose-dependent decrease of cell viability and mitochondrial membrane potentials whereas the apoptosis rate and caspase 3 activity showed a dose-dependent increase after rotenone treatment.Conclusion： Rotenone induces the apoptosis in dopaminergic cells by destroying mitochondrial membrane potentials in a concentration-dependent manner.
出处
《神经损伤与功能重建》
2008年第5期298-300,共3页
Neural Injury and Functional Reconstruction
关键词
鱼藤酮
凋亡
帕金森病
rotenone
apoptosis
Parkinson＇s disease
