补体在肠缺血再灌注损伤中的作用及机制  

Role and mechannism of complement in intestinal ischemia-reperfusion injury

作　　者：刘高科[1] 汪正清[1] 

机构地区：[1]第三军医大学基础部微生物学教研室,重庆400038

出　　处：《免疫学杂志》2010年第3期271-274,共4页Immunological Journal

基　　金：重庆自然科学基金(2007BB5011);国家自然科学基金(30471723)

摘　　要：肠缺血再灌注后补体经典途径、MBL途径和旁路途径有不同程度的活化,补体活化产物C3a、C4a、C5a和攻膜复合物(MAC)能引起组织炎症损伤,其机制有MAC介导的直接效应,有C3a、C5a和亚溶解数量的MAC刺激白细胞和血管内皮细胞产生一系列炎症介质,导致肠黏膜损伤,甚至累及远端器官功能障碍的间接效应。目前,已有多种补体抑制剂用于对肠缺血再灌注损伤的保护研究。After intestinal ischemia-reperfusion （I/R）, complement can be activated by the antibody-dependent classical pathway, the mannose-binding lectin （MBL） pathway, or the alternative pathway. Complement activation leads to release of the biologically active substance including C3a, C4a, C5a, and membrane attack complex （MAC）. These complement activation products can induce intestinal I/R injury directly or indirectly. Leukocytes and vascular endothelial cells could be directly activated by C3a, C5a, and MAC and release a series of inflammation mediators, resuhing in local intestinal mucosa injury. And also, the inflammation factors may harm distant organs. At present there are some specific inhibitors have been used to block complement activation to prevent intestinal injury after I/R.

关 键 词：补体 缺血再灌注 炎症 补体抑制剂 

分 类 号：R392[医药卫生—免疫学]