术后缺血再灌注时HMGB1的损伤机制及干预治疗进展  

Mechanism and Interference therapy of HMGB1 after Ischemia/ Reperfusion Injury

作　　者：赵强[1] 金振晓[1] 易定华[1] 冯关力[2] 

机构地区：[1]第四军医大学附属西京医院心血管外科,西安710032 [2]西安市中心医院,西安710003

出　　处：《国际外科学杂志》2009年第6期424-427,共4页International Journal of Surgery

基　　金：基金项目：陕西省科技攻关项目（No.2008K13-03）

摘　　要：器官移植及体外循环等术后伴随缺血再灌注损伤的发生，使活化的炎症细胞表达分泌HMGB1，并协同其他炎症因子产生机体损伤。其机制在于HMGB1可激活TLR、RAGE、TM等受体和NF—KB转录因子、P38MAPK旁路，导致HMGB1自身和其它炎症因子的进一步释放。与脓毒血症引起的分泌不同，缺血再灌注损伤引起的HMGB1出现较早，持续时间长。HMGB1的干预治疗，能有效减低缺血再灌注损伤引发的HMGB1释放。After operations such as organ transplantation or cardiopulmonary bypass complicated with ischemia/reperfusion injury, activated inflammatory cells can express and secret HMGB1, and cooperate with other inflammation factor to induce tissue damage. The mechanism is HMGB1 actives such receptors as TLRs, RAGE, TM, and NF-kB transcription factor, P38MAPK pathway, induce releasing of HMGBlitself and other inflammation factors . Different with sepsis, HMGBI emerges much earlier, lasting longer. Interference therapy of HMGBI could effectively decrease secretion of HMGBI after ischemia/reperfusion injury.

关 键 词：高迁移率族蛋白 缺血再灌注损伤 炎症因子 器官移植 体外循环 

分 类 号：R285.5[医药卫生—中药学]