蛛网膜下腔出血后早期脑损伤的信号通路  

Signaling pathway of early brain injury after subarachnoid hemorrhage

作　　者：王益朋 王小刚[1] 郭庚[1] 杨雯 Wang Yipeng;Wang Xiaogang;Guo Geng;Yang Wen(Department of Neurosurgery,the First Hospital of Shanxi Medical University,Taiyuan 030001,China;Department of Neurology,the First Hospital of Shanxi Medical University,Taiyuan 030001,China)

机构地区：[1]山西医科大学第一医院神经外科,太原030001 [2]山西医科大学第一医院神经内科,太原030001

出　　处：《国际脑血管病杂志》2019年第10期791-795,共5页International Journal of Cerebrovascular Diseases

基　　金：国家自然科学基金(81201991);中国博士后科学基金(2015M571068,2016T90115);山西省自然科学基金(201601D011127)。

摘　　要：早期脑损伤(early brain injury,EBI)是指动脉瘤性蛛网膜下腔出血后72 h内脑组织的直接损伤以及继发病理生理学改变。研究表明,多种信号通路参与了EBI的机制,例如Kelch样环氧氯丙烷相关蛋白-1(epoxy chloropropane Kelch sample related protein-1,Keap1)-核因子E2相关因子2(nuclear factor erythroid-2 related factor 2,Nrf2)-抗氧化反应元件(antioxidant response element,ARE)通路、Toll样受体4(Toll-like receptor 4,TLR4)/核因子-κB通路、磷脂酰肌醇3-激酶(phosphatidylinositol-3 kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)通路等。文章对涉及EBI的不同信号通路的作用机制进行了综述。Early brain injury(EBI)refers to the direct damage and secondary pathophysiological changes of brain tissue within 72 h after aneurysmal subarachnoid hemorrhage.Studies have shown that a variety of signaling pathways are involved in the mechanism of EBI,such as ecoxy chloropropane Kelch sample related protein-1(Keap1)-nuclear factor E2 related factor 2(Nrf2)-antioxidant response element(ARE)pathway,Toll-like receptor 4(TLR4)/nuclear factor-κB pathway,phosphatidylinositol-3 kinase(PI3K)/protein kinase B(Akt)pathway.This article reviews the mechanisms of action of different signaling pathways involved in EBI.

关 键 词：蛛网膜下腔出血 脑损伤 信号转导 

分 类 号：R73[医药卫生—肿瘤]