高迁移率族蛋白B1在血管性痴呆中的炎性作用机制及研究进展  

Inflammatory mechanism and research progress of high mobility group protein B1 in vascular dementia

作　　者：常光明[1] 陈潇(综述) 耿鑫(审校)[2] CHANG Guang;CHEN Xiao;GENG Xin(Laboratory Medical Center,General Hospital of Tianjin Medical University,Tianjin 300052, China;Basic Medical College,Tianjin Medical University,Tianjin 300070,China)

机构地区：[1]天津医科大学总医院检验中心,天津300052 [2]天津医科大学基础医学院,天津300070

出　　处：《国际检验医学杂志》2019年第15期1893-1896,共4页International Journal of Laboratory Medicine

基　　金：国家自然科学基金课题(81671054、81771135);天津市应用基础与前沿技术重点项目(19JCZDJC35600)

摘　　要：血管性痴呆是老年人痴呆的第二大常见原因,仅次于阿尔茨海默病,并且与年龄有关。高迁移率族蛋白B1(HMGB1)作为重要的损伤相关分子模式(DAMPs)的成分,不仅能启动早期的炎症反应,同时在晚期能促进炎症介质的释放,引起神经元的损伤,造成脑组织损伤。但同时也发现HMGB1具有促进脑血管修复的作用。Vascular dementia(VD)is the second most common cause of dementia in the elderly,second only to Alzheimer′s disease,and related to age.High mobility group protein B1(HMGB1),as an important component damage associated molecular patterns(DAMPs),can not only initiate early inflammatory response,but also promote the release of inflammatory mediators in the late stage,causing neuronal damage and brain tissue damage.However,it was also found that HMGB1 could promote cerebrovascular repair.

关 键 词：高迁移率族蛋白B1 血管性痴呆 炎症反应 

分 类 号：R446.1[医药卫生—诊断学]