鱼藤酮诱导多巴胺能细胞α-突触核蛋白聚集和ERK1/2通路活化的研究  

Research on rotenone-induced α-synuclein aggregation and ERK1/2 pathway activation in dopaminergic cells

作　　者：张振涛[1] 曹学兵[1] 王涛[1] 孙圣刚[1] 王岚[1] 徐丽[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院,湖北武汉430022

出　　处：《山东医药》2008年第22期1-2,共2页Shandong Medical Journal

基　　金：国家自然科学基金资助项目(30570627)

摘　　要：目的探讨鱼藤酮对多巴胺能细胞α-突触核蛋白聚集和细胞外信号调节激酶-1/2(ERK1/2)通路活化的影响。方法用鱼藤酮处理神经元样分化的PC12细胞,四甲基偶氮唑盐法检测细胞活力,免疫荧光法检测α-突触核蛋白聚集,免疫细胞化学法检测ERK1/2通路活化情况。结果鱼藤酮处理后细胞活力呈时间依赖性下降;磷酸化ERK1/2水平逐渐升高(P均<0.01);处理16 h后细胞内出现α-突触核蛋白聚集体,24 h后进一步增多。结论鱼藤酮可诱导α-突触核蛋白聚集和ERK1/2通路活化,参与多巴胺能神经元损伤。Objective To investigate the effect of rotenone on ct-synuclein aggregation and ERK1/2 pathway activation in dopaminergic cells. Methods PC12 cells differentiated by nerve growth factor were treated by rotenone. Cell viability was measured by mononuclear cell direc cytotoxicity assay, immunofluorescence was used to detect the aggregation of α-synuclein, and immunocytochemistry was used to detect the activation state of ERK1/2 pathway. Results After being exposed to rotenone , the cell viability declined in a time-dependent manner, pERK1/2 level rised gradually（P all〈 0.01 ）. Aggregation of α-synuclein was appeared after exposing to rotenone for 16 hours and increased exposing to rotenone for 24 hours. Conclusions Rotenone induces α-synuclein aggregation and ERK1/2 pathway activation in dopaminergic cells, which participate in the injury of dopaminergic cells.

关 键 词：鱼藤酮 Α-突触核蛋白 PC12细胞 细胞外信号调节激酶-1/2通路 帕金森病 

分 类 号：R742[医药卫生—神经病学与精神病学]