激肽释放酶神经保护作用的机制探索  

Mechanisms underlying neuroprotective roles of kallikrein in ischemic stroke

作　　者：唐宇平[1] 崔梅[1] 董强[1] 

机构地区：[1]复旦大学附属华山医院神经内科,上海200040

出　　处：《中国新药杂志》2011年第11期988-992,共5页Chinese Journal of New Drugs

基　　金：国家自然科学基金项目(30570632;81070935)

摘　　要：脑血管病发病率高,严重危害人类健康。探索缺血性脑损害的机制与阻断相应分子与细胞损害的环节是目前全世界神经科学工作者研究的焦点和热点。激肽释放酶-激肽系统(kallikrein-kinin system,KKS)是体内重要的炎性调节系统。综合探索KKS系统在脑缺血不同时期的作用,对缺血再灌注脑组织中激肽释放酶的动态变化进行系统的研究,从细胞内信号转导水平来探索B1和B2受体作用的深层机制,并进一步研究组织型激肽释放酶作用通路上新的相关蛋白分子及发现新的信号通路,这一系列的工作将对脑缺血的试验性治疗提供崭新的思路。Ischemic stroke is one of the most common diseases that cause unnatural death and disability. It is a hot spot to study the mechanisms likrein-kinin system （KKS） is a well and the molecular and cellar key link known inflammation regulatory system in cerebral ischemic damage. Kalthat plays an important role in the pathophysiologic process after cerebral ischemia. However, current researches implies that this system may produce completely different effects during various stages of cerebral ischemia. Therefore, it is important to study the roles of kallikrein-kinin system as well as bradykinin B1 and B2 receptors in cellar signal transduction after ischemic stroke, and to explore new target proteins in the kallikrein pathway. In this review, we reviewed the roles of KKS in various stages of cerebral ischemia, looking forward to provide promising targets for the treatment of ischemic stroke.

关 键 词：缺血性脑血管病 激肽释放酶-激肽系统 组织型激肽释放酶 B1和B2受体 

分 类 号：R741[医药卫生—神经病学与精神病学]