JNK/c-Jun信号通路对非酒精性脂肪性肝炎脂性凋亡的影响  

Influence of JNK/c-Jun Signaling Pathways for Lipoapoptosis of Non-Alcoholic Fatty Hepatitis

作　　者：马燕花[1] 邱晓青[2] 师霞[1] 徐三朋 

机构地区：[1]甘肃中医药大学,兰州730000 [2]甘肃中医药大学附属医院检验科,兰州730000

出　　处：《医学综述》2017年第9期1675-1679,1684,共6页Medical Recapitulate

基　　金：国家自然科学基金(81560753)

摘　　要：非酒精性脂肪性肝炎(NASH)是非酒精性脂肪性肝病的一个重要病理阶段,其可以发展为肝硬化,甚至肝细胞癌,对疾病的进展起决定性作用。对NASH发生、发展机制的研究普遍接受"二次打击"学说。其中,肝细胞脂毒性凋亡是NASH的一个重要病理组织学特征。c-Jun氨基端激酶(JNK)是丝裂原活化蛋白激酶家族的成员。JNK/应激活化蛋白激酶应激信号通路与NASH的发病机制密切相关,在NASH中多种应激刺激都能激活肝脏内的JNK信号通路,诱导细胞凋亡。Non-alcoholic steatohepatitis（NASH） is an important pathological stage of nonalcoholic fatty liver dis- ease. Because it can develop into cirrhosis, or even hepatocellular carcinoma, it plays a decisive role in the progression of the disease. The theory of ＂two hit＂ is accepted generally on the study of NASH occurrence and development mechanism. Among them, lipoapoptosis of hepatocytes is an important histopathological feature of NASH. C-Jun N-terminal kinase （JNK） is a member of the mitogen activated protein kinase family. JNK/SAPKs stress signaling pathway is closely related to the pathogenesis of NASH. In NASH, a variety of stresses can activate JNK signaling pathway and induce apoptosis in the liver.

关 键 词：非酒精性脂肪性肝炎 c-Jun氨基端激酶/c-Jun信号转导通路 脂性凋亡 

分 类 号：R575.1[医药卫生—消化系统]