MEK/ERK信号通路与脑缺血再灌注损伤

MEK/ERK Signaling Pathways and the Cerebral Ischemia-reperfusion Injury

在脑缺血病灶中,中心区神经元坏死为主,周围以缺血半暗带凋亡为主,抑制半暗带细胞的凋亡,可以减少细胞的死亡和脑梗死的面积,因此改善半暗带是治疗脑卒中的关键环节。目前发现MAPK分布于整个中枢神经系统中,MEK/ERK信号通路参与细胞生长、发育、细胞抗凋亡等过程,在脑缺血再灌注损伤过程中有MEK/ERK信号通路的参与,MEK/ERK通路通过影响Bcl-2家族成员的活化和表达调控内源性凋亡途径,ERK通过对细胞周期的调控,抑制胶质细胞大量活化和过度增殖,减少了有害因子并改善局部微循环,从而减少神经元的凋亡。可能为脑血管的防治开辟一条新的途径。本文就MEK/ERK信号通路的结构特点与脑缺血再灌注损伤相关作用机制作一综述。

In cerebral ischemia, neuron necrosis mainly occurred in central while ischemic penumbra apoptosis mainly occurred in around. Inhibiting penumbra cell apoptosis can reduce cell death and cerebral infarction area. Therefore improving penumbra is the key link in the treatment of cerebral stroke, MEK/ERK signaling pathways participate in cell growth development, and cell anti-apoptosis process, MEK/ERK signal path participation in cerebral ischemia reperfusion injury. This article will review the structure features of mek/erk signaling pathway and the mechanism of ischemia-reperfusion injury.