摘要
目的:探讨促红细胞生成素(erythropoietin,EPO)对1-甲基-4-苯基吡啶离子(MPP+)诱导的帕金森病细胞模型的保护作用。方法:使用MPP+处理PC12细胞,建立多巴胺能细胞损伤模型,使用不同浓度的EPO预处理细胞,四甲基偶氮唑盐(MTT)法检测细胞活力,流式细胞术检测细胞凋亡率,荧光酶标仪检测细胞内活性氧物质水平,比较各组间的差异。结果:MPP+处理后PC12细胞活力下降,250μmol/LMPP+处理24h后,细胞活性下降为对照组的39.64%,而EPO预处理组随着EPO浓度的增加,细胞活力逐渐上升,40U/mlEPO为促进细胞活力的最佳浓度。EPO预处理组细胞凋亡率明显低于单独MPP+组(P<0.01),且EPO预处理组的细胞内活性氧物质水平明显低于单独MPP+组(P<0.01)。结论:EPO对MPP+诱导的PC12细胞损伤具有保护作用,这种保护作用可能与其抗氧化应激作用有关。
Objective：To explore if the erythropoietin could have protective effects on Parkinsonism cell models induced by MPP^＋. Methods：MPP^＋ was added into the cultured PC12 cells to establish a cell model of Parkinson disease. The cells were pre-treated with EPO. MTT was used to assay the cell viability and metabolism state. Flow cytometry was employed to assay the apoptosis ratio, and the fluorescence microplate reader was used to detect the ROS. Results：After treated with 250 μmol/ L MPP^＋ for 24 h, the cell viability was declined to 39.64%. As the concentration of erythropoietin was increased, the cell viability of PC12 cells was increased simultaneously. 40U/ml EPO showed the greatest protective effect. The apoptosis ratio was significantly decreased in EPO pre-treated group than in MPP^＋ group and the same trend was noted in ROS generation. Conclusion： Erythropoietin can protect PC12 cells from MPP^＋ neurotoxicity, and this protective effect may relate to cleavage of the oxdative stress products.
出处
《神经损伤与功能重建》
2008年第2期77-79,121,共4页
Neural Injury and Functional Reconstruction
