缺血后适应脑保护机制的研究进展

摘要

Extending the thrombolysis time window and reducing reperfusion injury are problems urgently needed to be solved in ischemic cerebrovascular disease. Ischemic postconditioning provides a possible solution, which has been becoming a hot research topic. Postconditioning, which refers to a series of brief occlusions and reperfusions of the blood vessels, is conducted after ischemia/reperfusion. Postconditioning can induce organ's endogenous protective effects against ischemia reperfusion(I-R) injury. This article will discuss the neuroprotective mechanism of ischemic postconditioning: reduction of brain blood flow changes after I-R, attenuation of ROS production and apoptosis, anti-inflammatory, and changes in pathways involved in neuronal death after stroke.%如今延长溶栓时间窗、减轻再灌注损伤是缺血性脑血管病亟待解决的的问题，缺血后适应提供了一种可能的解决方法，故成为研究的热点。缺血后适应通常指的是在组织缺血-再灌注之后进行的一系列短暂血管闭塞/血管再灌注，诱导组织针对缺血-再灌注损伤产生内源性保护作用，减少组织器官缺血-再灌注损伤。该文将综述缺血后适应脑保护的基本机制：减少缺血-再灌注后脑血流的改变，减少氧化应激产物的产生，抗炎，相关信号传导通路改变。