脑缺血后适应脑保护的研究进展  

Progress in brain protection with ischemic postconditioning

作　　者：张川荛[1] 李树清[1] 

机构地区：[1]昆明医学院病理生理教研室,云南昆明650500

出　　处：《中国病理生理杂志》2011年第5期1025-1028,1040,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30660056;No.30971171);教育部博士点专项科研基金资助项目(No.20050678008)

摘　　要：近年的研究发现,心梗病人血运重建后的头几分钟多次阻塞、再灌注,便可获得与缺血预适应（is-chemic preconditioning,IP）相同的效果,即缺血后适应（ischemic postconditioning,PC）,类似于动物心脏研究所见。由此断定，缺血PC是一种在方法上与IP完全不同，但效果基本一致的细胞保护措施。缺血PC的发现提示：机体缺血状态下，内部天然内源性保护机制的激活对机体的抗损伤反应具有特殊的生物学意义[1]。Cerebrocardiovascular diseases and stroke are serious threat to human health.More attentions focus on cerebral ischemia and the publications suggest that ischemic preconditioning prevents ischemic myocardium from ischemia/reperfusion injury,soon followed by preconditioning against cerebral ischemic injury.However,in clinical management,ischemia is often unpredictable.In recent years,researchers found that ischemic postconditioning and ischemic preconditioning obtained the similar effects on brain protection after cerebral ischemia.The endogenous protective mechanisms play a key role in protecting against brain ischemic injury.As a novel manner to protect against brain injury,postconditioning attenuates the infarct volume following brain ischemia/reperfusion and prompts the neurological recovery by prolonging the therapeutic time window.This article reviews the processes of ischemic,hypoxia,hypothermia and pharmacologic postconditioning,and the possible brain protection mechanisms activated by the signal transduction of serine/threonine kinase（Akt）,phosphatidylinositol 3-kinase（PI3K）,mitogen-activated protein kinase（MAPK）,protein kinase C（PKC）,and ATP-sensitive potassium channel（KATP） pathways.

关 键 词：脑缺血 后适应 脑保护 

分 类 号：R743.1[医药卫生—神经病学与精神病学] R363.2[医药卫生—临床医学]