缺血性肝炎的相关发病机制  

The pathogenesis of ischemic hepatitis

作　　者：李钟霖 王玮珺 杨玲[1] Li Zhonglin;Wang Weijun;Yang Ling(Department of Gastroenterology,Affiliated Union Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430032,China)

机构地区：[1]华中科技大学同济医学院附属协和医院消化内科,武汉430022

出　　处：《中华肝脏病杂志》2021年第7期705-710,共6页Chinese Journal of Hepatology

摘　　要：缺血性肝炎是由于心脏的低排出量或感染性休克而导致的肝脏细胞因缺血缺氧而发生坏死所产生的炎症,其常并发于心力衰竭患者和重度呼吸道感染患者等。缺血性肝炎的发病机制一方面是由于缺血缺氧导致的肝细胞损伤,释放damage-associated molecular patterns(DAMPs),与细胞表面如Toll样受体等结合引起炎症反应;另一方面是由于当缺血的肝脏再次恢复血供时,肝细胞线粒体产生大量ROS,造成二次损伤,即缺血再灌注损伤。现对这两种机制及相关的分子通路进行阐述。Ischemic hepatitis is inflammation caused by necrosis of liver cells due to ischemia and hypoxia caused by low cardiac output or septic shock.It is often complicated by heart failure or severe septic shock.One of the pathogenesis of ischemic hepatitis is hepatocyte injury caused by ischemia and hypoxia,which results in damage-associated molecular patterns(DAMPs)release and binding to membrane receptors such as toll like receptors(TLRs)to cause inflammatory reactions.The other is when the ischemic liver is reperfused,hepatocyte mitochondrias will produce a large amount of ROS causing ischemia reperfusion injury.These two mechanisms and related molecular pathways are elaborated in this paper.

关 键 词：肝炎 缺血性肝炎 肝脏缺血缺氧损伤 肝脏缺血再灌注损伤 

分 类 号：R575.1[医药卫生—消化系统]