Fas/FasL在急性胰腺炎肝损伤中的作用  

Role of Fas/FasL in acute pancreatitis-associated liver injury

作　　者：张晓华[1] 袁柏思[1] 朱人敏[1] 

机构地区：[1]中国人民解放军南京军区南京总医院消化内科,江苏省南京市210002

出　　处：《世界华人消化杂志》2008年第15期1661-1665,共5页World Chinese Journal of Digestology

摘　　要：Fas/FasL介导的凋亡参与急性胰腺炎肝损伤的发生发展,急性胰腺炎上调肝内的促凋亡通路并且促使肝细胞损伤和肝细胞凋亡.急性胰腺炎时通过上调Kupffer细胞内FasL生成的信号使FasL表达增加,FasL激活Fas相关的死亡域和暴露死亡效应结构域,随后活化Caspase级联反应和下游的效应Caspases,最终导致DNA裂解和肝细胞凋亡,从而介导肝损伤.本文就Fas/FasL结构、分布、功能及介导急性胰腺炎肝损伤的机制作一综述.Fas/FasL-mediated apoptosis is involved acute pancreatitis-associated liver injury. It upregulates proapoptotic pathways in the liver and promotes hepatocytic injury as well as hepatocytic apoptosis during acute pancreatitis. The signal of the production of FasL and the expression of FasL were up-regulated in kupffer ceils during acute pancreatitis. Then, FasL activates Fas-associated death domain （FADD） and unmasks its death effector domain （DED） followed by subsequent activation of the Caspase cascade and downstream effector Caspases, ultimately resulting in DNA cleavage and hepatocytic apoptosis. This review aimed to elucidate the construction, distribution and function of Fas/FasL, and to highlight mechanism of acute pancreatitis-associated liver injury mediated by Fas/FasL.

关 键 词：FAS/FAS配体 急性胰腺炎 肝损伤 凋亡 

分 类 号：R576[医药卫生—消化系统]