缺血后处理是一种可以减轻脑缺血再灌注损伤的新方法,对脑缺血的再灌注损伤也具有显著保护作用。通过抑制基因过表达,调控炎症、凋亡及氧化应激、自我吞噬,影响泛连接蛋白1/P2X7嘌呤受体复合物途径、p38 MAPK-ATF2通路作用,下调AQP4的表达等机制,其改善了血管神经单元细胞的相互作用,实现神经系统的保护作用。脑缺血是危害人类健康的常见病、多发病,其较高发病率、病死率和致残率给社会、家庭带来沉重的负担和痛苦。研究者发现脑组织经过一定时间的缺血后再次恢复血液灌注时其功能及结构损伤反而会加重,即“脑缺血再灌注损 Ischemic postconditioning is a new method that can relieve cerebral ischemia-reperfusion injury and has a significant protective effect on cerebral ischemia-reperfusion injury. Mechanisms such as inhibition of gene overexpression, regulation of inflammation, apoptosis and oxidative stress, self-phagocytosis, effects of the pancrelixin 1 / P2X7 purinergic receptor complex pathway, p38 MAPK-ATF2 pathway, and down-regulation of AQP4 expression have improved Vascular neural cell interactions, to achieve the neuroprotective effect. Cerebral ischemia is a common disease endangering human health, frequently-occurring disease, its high morbidity, mortality and disability rate to the community, families, a heavy burden and pain. The researchers found that after a certain period of time after the brain tissue ischemia and blood flow to resume its function and structural damage but will aggravate, that is, ”cerebral ischemia-reperfusion injury