高迁移率族蛋白B1在缺血性脑卒中的作用及研究进展  

Progress of high mobility group box B1 and its relationship in stroke

作　　者：金聪丽 周海红[1] 

机构地区：[1]广东医学院附属医院神经内科,湛江524023

出　　处：《中华诊断学电子杂志》2016年第4期284-287,共4页Chinese Journal of Diagnostics(Electronic Edition)

基　　金：广东省科技计划项目(2011B031800390)

摘　　要：脑卒中后预后很大程度受炎症的影响,高迁移率族蛋白B1(HMGB1)作为促炎因子,参与了神经系统疾病的发生发展,其中在缺血性脑卒中,HMGB1贯穿动脉粥样硬化形成、脑卒中发生、脑卒中修复整个过程,并扮演着了不同的角色。HMGB1通过增加内皮通透性,促炎作用以及促进平滑肌迁移等参与了动脉粥样硬化发展。坏死神经元释放的HMGB1不仅反向导致神经元的坏死,并且作为危险相关分子模式(DAMP)分子放大炎症反应。然而星形胶质细胞通过释放HMGB1增加内源性内皮组细胞(EPCs)的活力,促进脑卒中后的神经血管修复。笔者就HMGB1的结构、功能以及缺血性脑卒中的作用及研究进展做一综述。Inflammatory cascades have a major impact on outcome and regeneration after ischemic stroke.High mobility group box B1 （HMGB1）,a pro-inflammatory cytokine,contributes to the development of atherosclerosis,ischemic brain injury, and neurovascular repair. Meanwhile, it plays a very different role in stroke.HMGB1 participates in progression of atherosclerosis through vascular endothelial hyperpermeability, harmful inflammatory response and migration of smooth muscle cells.HMGB1 is released by necrotic neuronal cells,not only reverses to injury neuronal cell, but as danger-associated molecular patterns （ DAMP ） to amplify inflammatory response. On the other hand, astrocyte-derived HMGB1 induces the promotion of endogenous EPCs viability and enhances neurovascular repair in post-ischemic.This review mainly focuses on the present research of HMGB1 structure,functions and relationship in stroke.

关 键 词：脑卒中 高迁移率族蛋白质类 动脉粥样硬化 

分 类 号：R743.3[医药卫生—神经病学与精神病学]