α-突触核蛋白促进MES23.5细胞突起生长

摘要

Objective To investigate the effect of ct-synuclein(α-syn) on the neurite outgrowth of MES 23. 5 dopaminergic cells. Methods The neurite length of MES 23.5 cells were measured at different time points after addition of recombinant human et-syn to the culture medium. Double immunofluorescent labeling was used to examine the co-localization of et-syn and β-tubulin in the cells. ELISA was applied to analyze the p-tubulin levels in the cells. Results The mean neurite length of the α-syn-treated cells was significantly longer than that of control neurons at 1 h, 4 h and 24 h after addition of α-syn. The effect of α-syn on neurite outgrowth was reversed by P-tubulin inhibitor, colchicine. Α-Syn and p-tubulin were shown to colocalize in the cells, and the levels of β-tubulin was higher in the a-syn-treated cells than in control cells. Conclusion α-Syn can promote neurite outgrowth of MES23. 5 dopaminergic cells possibly by its effect on tubulin synthesis and microtubule assembly.%目的 研究人α-突触核蛋白(α-synuclein,α-syn)对MES23.5多巴胺能神经细胞突起生长的作用.方法 MES23.5细胞外添加α-syn蛋白,测定不同时间细胞突起的长度；免疫荧光双重标记法观察α-syn与β-微管蛋白之间的相互关系；ELISA方法检测细胞内β-微管蛋白含量.结果 α-Syn处理组神经元突起的平均长度及β-微管蛋白的含量在培养l、4和24h时均明显大于对照组；α-Syn的这、作用可被微管蛋白抑制剂秋水仙碱阻断；α-Syn与β-微管蛋白在细胞内共存.结论 α-Syn具有促进MES23.5多巴胺能神经细胞突起生长的作用,该作用很可能通过影响微管蛋白的合成及微管的组装来完成.