Abstract
Kitagawa等[1]在沙土鼠脑缺血的实验研究中,首次观察到机体对短暂亚致死性缺血的适应性反应能增加神经元对致死性缺血的耐受性,由此提出了脑缺血预处理(ischemic preconditioning, IP)的概念.此后各国学者对IP的机制进行了广泛的研究,提出了许多假说.近年来,以受体激活为起点,以细胞内信号转导为主线,构成预处理保护机制研究的重点,其中丝裂原激活的蛋白激酶(mitogen activated protein kinase, MAPK)途径在IP中的作用引起了人们的关注。
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