过氧化物酶体增殖物激活受体α、γ调控长链酰基辅酶A合成酶1对肝纤维化进程的影响  

Studies on PPAR α and γ participating in progression of liver fibrosis by regulating ACSL1

作　　者：辛萱[1,2] 颜红柱[1] 李维卿[1] 余宏宇[1] 

机构地区：[1]第二军医大学长征医院病理科,上海200003 [2]济南军区总医院病理科,济南250031

出　　处：《临床肝胆病杂志》2014年第7期700-702,共3页Journal of Clinical Hepatology

摘　　要：在肝纤维化的发生发展进程中,过氧化物酶体增殖物激活受体(PPAR)α、γ具有调控脂代谢、脂肪酸代谢和抗肝纤维化等生物学功能,并与调控脂肪代谢的相关酶类关系密切。长链酰基辅酶A合成酶1(ACSL1)作为脂肪代谢的关键酶之一,在肝脏中参与脂质的合成与分解代谢,可引起肝脏内脂质沉积、炎症反应,并在肝脏中直接或间接促进肝纤维化进程。回顾了PPARα、γ和ACSL1各自的生物学功能与作用;简述了PPARα、γ对ACSL1的转录调控机制;从肝脏脂代谢和肝星状细胞活化等两个方面分析了PPARα、γ对ACSL1的调控作用,进而影响肝纤维化进程。从而指出在肝脏中PPARα、γ通过调控ACSL1直接或间接参与肝纤维化进程。During the development and procession of liver fibrosis, peroxisome proliferator-activated receptor （PPAR） α and νare in charge of the regulation of lipid metabolism, fatty acid metabolism, anti - liver fibrosis, etc. , and are closely related to fat metabolism - related enzymes. As a key enzyme in fat metabolism, acyl - CoA synthetase long - chain family member 1 （ ACSL1 ） is involved in lipid synthesis and catabolism and then causes lipid deposition and inflammation in the liver, so it directly or indirectly promotes hepatic fibrosis. The biological functions and roles of PPAR α and ν, and ACSL1 are reviewed ; the action mechanisms of PPAR α and ν in the transcriptional regulation of ACSL1 are briefly described ; the regulatory effects of PPAR α and ν on ACSL1 and their effects on the progression of hepatic fibrosis are analyzed from the aspects of liver lipid metabolism and hepatic stellate cell activation. It is pointed out that in the liver PPAR α and ν are directly or indirectly involved in the progression of hepatic fibrosis by regulating ACSL1.

关 键 词：PPARΑ PPARν 酰基辅酶A 肝硬化 综述 

分 类 号：R575.2[医药卫生—消化系统]