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.
出处
《山东医药》
CAS
北大核心
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)
