α-硫辛酸通过激活ERK信号通路促进神经突触生长  

α-Lipoic acid promotes neurite outgrowth via activating ERK signaling pathway

作　　者：朱维娜[1] 王晓辉[2] 丁正年[2] 刘莉[2] 李跃华[1] 

机构地区：[1]南京医科大学病理生理学系,江苏省210029 [2]南京医科大学第一附属医院

出　　处：《江苏医药》2012年第12期1368-1370,共3页Jiangsu Medical Journal

基　　金：国家自然科学基金(30972856;81071752;81071067);江苏省自然科学基金(BK2008467);江苏省六大人才高峰(07-B-041)

摘　　要：目的探讨α-硫辛酸(LA)促进神经突触生长的可能机制。方法将体外培养的小鼠神经母细胞瘤N2a细胞分为对照组(A组)、细胞外信号调节蛋白激酶(ERK)抑制剂PD98059 40μM组(B组)、LA 500μM组(C组)和PD98059 40μM+LA 500μM组(D组)。用光学显微镜观察细胞突触生长情况,Western blot法检测ERK表达水平。结果与A组相比,C组突触生长、ERK激活水平增加(P<0.01);而D组能明显抑制C组上述观察指标的增加过程(P<0.01)。结论 LA对神经细胞突触生长的促进作用可能是通过激活ERK依赖性信号通路来实现的。Objective To investigate the possible mechanism of neurite outgrowth induced by a-lipoic acid（LA）. Methods The mouse neuroblastoma N2a cells in vitro were divided into four groups of A（normal controls） ,B（pretreated with ERK inhibitor PD98059 40 μM） ,C（stimulated with LA 500μM） and D（pretreated with PD98059 40 μM and then stimulated with LA 500μM）. The neurite outgrowth was observed under light microscope, and the ERK activation was detected by Western blot. Results Compared with group A, the neurite outgrowth and level of ERK activation were significantly increased in group C（P〈0. 01）, which were all obviously inhibited in group D （P〈0. 01）. Conclusion LA-induced neurite outgrowth is mediated by the activation of ERK signaling pathway.

关 键 词：Α-硫辛酸 细胞外信号调节蛋白激酶信号通路 突触生长 

分 类 号：R363[医药卫生—病理学]