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缺血后处理可以诱导脑缺血耐受形成而产生脑保护作用,其机制可能与内源性生成物如腺苷和一氧化氮增多,氧自由基导致细胞脂质过氧化作用的减轻,细胞内信号转导通路的激活,线粒体的三磷酸腺苷敏感性钾通道开放和线粒体通透性转换孔道的关闭,脑缺血再灌注皮质内HSP70的表达增加有关。现对缺血后处理脑保护作用的研究现状做一综述。
Ischemic postconditioning can induce the formation of cerebral ischemic tolerance and produce a protective effect of the brain, its mechanism may be related to endogenous products such as adenosine and nitric oxide increased, oxygen free radicals lead to the reduction of cell lipid peroxidation, cells Activation of the internal signal transduction pathway, the opening of mitochondrial ATP-sensitive potassium channel and the closure of mitochondrial permeability transition pore, and the increase of HSP70 expression in cerebral ischemia-reperfusion cortex. The current research on the protective effect of ischemic postconditioning is summarized.