Sevoflurane Post-treatment Enhanced Mitochondrial Autophagy Through The HIF-1α/BNIP3 Pathway To Protect Against Myocardial Ischemia-reperfusion Injury

Objective:To observe the effect of SpostC on HIF-1α/BNIP3-mediated changes in mitochondrial autophagy at H/R,and to explore the related mechanism of SpostC regulating mitochondrial autophagy through HIF-1α/BNIP3 channel for myoc-ardial protection.Methods:H9C2 rat cardiac myocytes were randomly divided into 5 groups for culture:normal control group,hypoxia/reoxygenation group(H/R),hypoxia/reoxygenation+sevoflurane group(H/R+SPostC),hypoxia/reoxygenation+2ME2 group(H/R+2ME2),hypoxia/reoxygenation+sevoflurane+2ME2 group(H/R+SPostC+2ME2).T he cell viability,apo-ptosis rate,expression levels of HIF-1α and BNIP3 in cells,and the survival of aut-ophagosomes were observed.Results:Compared with H/R+SPos tC,cell viability of H/R+SPostC+2ME2 group decreased(1.125±0.013 vs 0.919±0.031,P<0.01),cell apoptosis rate increased(12.067±1.250 vs 20.233±0.503,P<0.01),HIF-1α,BNIP3 protein expressi-on level decreased(0.918±0.114 vs 0.487±0.164,P<0.05,0.738±0.059 vs 0.606±0.041,P<0.05).Conclusions:When cardiomyocytes are injured by H/R,HIF-1α is activated and BNIP3 expression is increased,which enhances mitoch-ondrial autophagy and cell su-rvival rate.Sevoflurane post-treatment can increase HIF-1α activationat H/R,overex-pression of BNIP3,enhance mitochondrial autophagy,thereby increasing cell survivalrate and protecting cardiomyocytes.