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脑缺血预处理及后处理均可以诱导脑缺血耐受形成而产生神经保护作用。二者的保护效应相当,其中的保护机制可能存在相似之处。如均依赖于相同的触发因子、介质和相同的信号转导通路,最终的效应器也是共同的。二者产生的保护作用可能与内源性生成物如腺苷和一氧化氮增多、磷酯酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶和细胞外信号调节激酶1/2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有关。
Cerebral ischemic preconditioning and postconditioning can induce cerebral ischemic tolerance formation and produce neuroprotective effects. The two have similar protective effects and similar protection mechanisms may exist. As both rely on the same trigger, mediator and same signaling pathway, the final effectors are also common. The protective effects of the two may be related to the increase of endogenous products such as adenosine and nitric oxide, activation of phosphatidylinositol 3-kinase / serine-threonine protein kinase and extracellular signal-regulated kinase 1/2, Mitochondrial adenosine triphosphate sensitive potassium channel opening and mitochondrial permeability transition pore closure.