肝脏缺血再灌注损伤与细胞凋亡  

Hepatic Ischemia Reperfusion Injury and Apoptosis

作　　者：王阳阳[1] 冯志杰[1] 郝晓[1] 

机构地区：[1]河北医科大学第二医院消化内科,河北省石家庄市050000

出　　处：《中国全科医学》2007年第19期1660-1663,共4页Chinese General Practice

摘　　要：肝脏缺血再灌注损伤是肝脏缺血再灌注后肝脏功能障碍和结构损伤加重的现象,研究表明,细胞凋亡是肝脏缺血再灌注损伤的重要机制之一,其与各种活性氧的生成、线粒体通透性改变、内质网应激和钙超载等机制有关。应用蛋白水解酶抑制剂、抗氧化剂、一氧化氮、一氧化碳、血红素氧合酶-1及抗凋亡基因疗法等可抑制细胞凋亡而减轻肝脏缺血再灌注损伤。Hepatic ischemia reperfusion injury is the aggravation of liver function or structure damages after hepatic is chemia reperfusion. Some studies have showed apoptosis may be one of the crucial mechanisms of hepatic ischemia reperfusion injury, which is associated with production of reactive oxygen species, mitochondrial permeability transition, endoplasmic reticulum stress and calcium overload. Proteolytic enzyme inhibitor, antioxidant, nitrogen monoxide, carbon monoxide, heme oxygenase-1 and anti-apoptosis gene therapy can reduce the iscbemia reperfusion injury by inhibiting apoptosis.

关 键 词：再灌注损伤 肝脏 细胞凋亡 

分 类 号：R575[医药卫生—消化系统]