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

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mTOR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-mTOR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mTOR有关。

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

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 mRNA-targeting 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.