腺苷酸活化蛋白激酶:炎症调控新靶点  

AMPK:a novel target controlling inflammation

作　　者：姚烽[1,2] 汲广岩[1] 张力[2] 

机构地区：[1]重庆医科大学临床学院,重庆400016 [2]重庆医科大学病理生理学教研室,重庆400016

出　　处：《生理学报》2012年第3期341-345,共5页Acta Physiologica Sinica

基　　金：supported by the National Natural Science Foundation of China (No. 30900651);the Education Commission of Chongqing Municipality;China (No. KJ090304)

摘　　要：腺苷酸活化蛋白激酶(AMP-activated protein kinase, AMPK)是参与调节糖、脂肪和蛋白质的代谢,维持细胞能量稳态的关键丝氨酸/苏氨酸蛋白激酶。新近研究表明:AMPK可通过磷酸化SIRT1、PGC-lα、p53和FoxO3a等下调核因子-κB的活性、抑制炎症相关基因的表达并减轻组织炎症损伤;此外,临床常用的降糖药二甲双胍也可通过激活AMPK而减轻炎症损伤。因而,AMPK将成为极具前景的抗炎药物开发新靶点。本文就AMPK的炎症调控效应及其分子机制作一综述。The AMP-activated protein kinase（AMPK） is a pivotal serine/threonine kinase participating in the regulation of glucose,lipid as well as protein metabolism and maintenance of energy homeostasis.Recent studies demonstrated that AMPK can also inhibit nuclear factor-κB,suppress the expression of inflammatory genes and attenuate inflammatory injury through phosphorylating its downstream targets including SIRT1,PGC-lα,p53 and FoxO3a.In addition,the widely used antidiabetic metformin also exerts its antiinflammatory effects through activating AMPK.Therefore,AMPK is emerging as a promising novel target for the development of anti-inflammatory drugs.This review summarized the anti-inflammatory effects ofAMPK and the underling molecular mechanisms.

关 键 词：腺苷酸活化蛋白激酶 炎症 核因子-ΚB 二甲双胍 

分 类 号：R363[医药卫生—病理学]