巨噬细胞移动抑制因子通过调控自噬抗H9c2心肌细胞缺氧/复氧损伤  

Macrophage migration inhibitory factor protects H9c2 cardiac myocytes against hypoxia/reoxygenation injury through regulation of autophagy

作　　者：李金玉 黄丹梅 张艳美[2] 石刚刚[2] 汪彬 LI Jinyu;HUANG Danmei;ZHANG Yanmei;SHI Ganggang;WANG Bin(Drug Clinical Trial Institution, the Second Affiliated Hospital;Department of Pharmacology, Shantou University Medical College, Shantou 515041, Guangdong, China)

机构地区：[1]汕头大学医学院第二附属医院国家药物临床试验机构办公室 [2]汕头大学医学院第二附属医院药理学教研室

出　　处：《中国临床药理学与治疗学》2018年第5期531-535,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：国家自然科学基金-广东省自然科学基金联合资助基金项目(U0932005);国家自然科学基金(81473215;81773729;81703508)

摘　　要：目的:研究巨噬细胞移动抑制因子(macrophage migration inhibitory factor,MIF)对H9c2心肌细胞缺氧/复氧(hypoxia/reoxygenation,H/R)过程中自噬的影响,并探讨其分子作用机制。方法:利用MIF特异性siRNA瞬时转染H9c2心肌细胞,建立H9c2心肌细胞H/R损伤模型,给予自噬经典抑制剂3-甲基嘌呤(3-MA),蛋白免疫印迹(Western blot)检测MIF、LC3、Cleaved caspase-3以及m TOR蛋白的表达。结果:干扰MIF后可抑制H/R诱导的心肌细胞自噬;自噬抑制剂3-MA抑制H/R诱导的心肌细胞自噬,减少细胞凋亡的发生;沉默MIF后可增加H/R过程中p-m TOR的表达。结论:MIF可通过抑制自噬减少H9c2心肌细胞H/R损伤,其作用机制可能与激活m TOR有关。AIM： To investigate the effects of macrophage migration inhibitory factor（ MIF） on autophagy of H9c2 cardiac myocytes during hypoxia/reoxygenation（ H/R） injury so as to explore the molecular mechanism. METHODS： The MIF mRNAtargeting siRNA was transfected to H9c2 cardiac myocytes. The H/R models of H9c2 cardiac myocytes were established. The autophagy inhibitor 3-methyladenine（ 3-MA） was added. The levels of MIF,LC3,Cleaved caspase-3 and mTOR protein expression in H9c2 cardiac myocytes were detected by Western blot. RESULTS： MIF siRNA transfection inhibited H/R-induced autophagy. The inhibitor of autophagy 3-MA suppressed H/R-induced autophagy and decreased apoptosis. MIF knockdown increased the expression of p-mTOR during H/R. CONCLUSION： MIF inhibits autophagy in H9c2 cardiomyocytes subjected to H/R,which is related to active mTOR protein.

关 键 词：巨噬细胞移动抑制因子 缺氧/复氧 H9C2心肌细胞 自噬 凋亡 

分 类 号：R965.2[医药卫生—药理学]