国际外科学杂志
國際外科學雜誌
국제외과학잡지
INTERNATIONAL JOURNAL OF SURGERY
2009年
6期
424-427
,共4页
赵强%金振晓%易定华%冯关力
趙彊%金振曉%易定華%馮關力
조강%금진효%역정화%풍관력
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
高遷移率族蛋白%缺血再灌註損傷%炎癥因子%器官移植%體外循環
고천이솔족단백%결혈재관주손상%염증인자%기관이식%체외순배
high mobility group box 1 (HMGB1)%ischemia/reperfnsion injury%inflammation factors%organ transplantation%cardiopulmonary bypass
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-κB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汴损伤引发的HMGB1释放.
器官移植及體外循環等術後伴隨缺血再灌註損傷的髮生,使活化的炎癥細胞錶達分泌HMGB1,併協同其他炎癥因子產生機體損傷.其機製在于HMGB1可激活TLR、RAGE、TM等受體和NF-κB轉錄因子、P38MAPK徬路,導緻HMGB1自身和其它炎癥因子的進一步釋放.與膿毒血癥引起的分泌不同,缺血再灌註損傷引起的HMGB1齣現較早,持續時間長.HMGB1的榦預治療,能有效減低缺血再灌汴損傷引髮的HMGB1釋放.
기관이식급체외순배등술후반수결혈재관주손상적발생,사활화적염증세포표체분비HMGB1,병협동기타염증인자산생궤체손상.기궤제재우HMGB1가격활TLR、RAGE、TM등수체화NF-κB전록인자、P38MAPK방로,도치HMGB1자신화기타염증인자적진일보석방.여농독혈증인기적분비불동,결혈재관주손상인기적HMGB1출현교조,지속시간장.HMGB1적간예치료,능유효감저결혈재관변손상인발적HMGB1석방.
After operations such as organ transplantation or cardiopulmonary bypass complicated with is-chemia/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-κB transcription factor,P38MAPK pathway,induce releasing of HMGB1 itself and other inflammation factors.Different with sepsis,HMGB1 emerges much earlier,lasting longer.Inter-ference therapy of HMGB1 could effectively decrease secretion of HMGB1 after ischemia/reperfusion injury.
