P13K／Akt信号转导通路与脑缺血后细胞凋亡

PI3K/Akt signal transduction pathway and apoptosis after cerebral ischemia

细胞凋亡为脑缺血时细胞死亡的重要形式之一.磷脂酰肌醇-3激酶（phosphoinositide-3 kinase,PI3K）/丝氨酸-苏氨酸蛋白激酶（serine/threonine kinase,Akt）为重要的细胞存活信号通路,c-Jun氨基端激酶（c-jun N-terminal kinase,JNK）为重要的促进细胞凋亡信号通路.这两大通路转导信号的动态平衡维持着生理状态下的细胞生存与凋亡.脑缺血刺激打破了这一生理平衡,导致大量神经细胞凋亡.多种确切的神经保护因素都与增强细胞存活信号的放大或抑制凋亡信号的放大有关,从而维持这2个通路信号的平衡.

Apoptosis is one of the important forms during cerebral ischemia.Phosphoinositide-3 kinase （PI3K）/serine/threonine kinase （Akt） is the important cell survival signaling pathway,while c-jun N-terminal kinase （JNK） is the important pro-apoptotic signaling pathway.The dynamic equilibrium of the two signal transduction pathways maintains cell survival and apoptosis under the physiological state.Stimulation during cerebral ischemia breaks this physiological balance and results in the apoptosis of massive neurons.A variety of proved neuroprotective factors are associated with the amplification of enhancement of cell survival signal or inhibition of apoptosis signal,and thrus maintain the balance between the two signal pathways.