摘要
脑缺血再灌注损伤可诱导神经元的凋亡,但确切的机制还不清楚。在脑缺血损伤过程中,Caspase家族、Bc l-2家族、Fas/Fasl、P38MAPK、CHOP等基因被诱导和表达。Caspase家族各基因参与缺血神经元凋亡的信号传导,其中Caspase-3是凋亡信号转导通路中最重要的蛋白酶。Bc l-2基因家族包括促凋亡和抑凋亡基因,这两种基因相互协调,共同对缺血神经元的凋亡进行调控。Fas/Fasl、P38MAPK、CHOP等基因的过表达诱导缺血神经元的凋亡,可能参与缺血神经元凋亡的信号传导机制。
Cerebral ischemia/reperfusion induces apoptesis in neuronal cells, but the mechanism is not well undemtood. Many apoptesis-associated genes,including Caspase family, Bcl-2 family, Fas/Fas1, P38MAPK and C/ EBP homologus protein （CHOP） are overexpressed during cerebral ischemia/reporfusion. Caspase family genes take part in signal conduction pathway of apoptesis of ischemic neurons, and caspase-3 is the most important protease in this signal conduction pathway. Bcl-2 family genes are composed of proapoptotic and antiapoptotic genes, which interact and mediate ischemia-induced neuronal cell apoptesis. Overexpression of Fas/Fas1, P38MAPK, CHOP contributes to ischemia-induced neuronal cell death and is presumedly involved in mechanism of signal conduction in ischemia neurons apoptosis.
出处
《解剖科学进展》
CAS
2006年第1期52-56,共5页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金资助项目(No.619019)
