摘要
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。
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.
出处
《神经药理学报》
2013年第4期29-34,共6页
Acta Neuropharmacologica
基金
遵义市科技局与遵义医院科技合作项目(No.2010017)
关键词
缺血后适应
缺血-再灌注损伤
脑保护
ischemic postconditioning
ischemina-reperfusion injury
neroprotection
