Mechanism Of PI3K/Akt Pathway Regulating Mitochondrial OPA1 And Drp1 In Sevoflurane Postconditioning Alleviating Myocardial Ischemia-reperfusion Injury

Objective: To investigate whether sevoflurane postconditioning can reduce myocardial ischemia-reperfusion injury by regulating mitochondrial OPA1 and drp1 through PI3K / Akt pathway.Methods: H9c2 rats were randomly divided into four groups:normal control group(Group C),hypoxia reoxygenation group(H / R group),sevoflurane postconditioning group(spostc group),PI3 K / Akt inhibitor + sevoflurane postconditioning group(YSP group).Group C: normal culture in CO2 incubator for 48 h without any intervention;group H / R: culture for 48 h,hypoxia for 3h,reoxygenation for 3h;group spotsc: culture for 48 h,hypoxia for 3 h,then treat with 2.4% sevoflurane for 15 min,and then take it out and continue to culture in CO2 incubator for 165 min;group YSP:normal culture in CO2 incubator for 40 h,and then culture the cells in the medium containing 10 μ M LY294002 for 8 hours.CCK-8 method was used to detect cell survival rate;flow cytometry was used to detect cell apoptosis;confocal microscope was used to observe mitochondrial morphology;pqrt-pcr was used to detect the m RNA expression levels of HIF-1 α,OPA1,drp1,AKT1;Western blotting was used to detect the protein expression levels of HIF-1 α,OPA1,drp1,AKT1 and phosphorylated Akt(p-Akt).Results:Compared with the hypoxia-reoxygenation group(H/R group),the survival rate of cardiomyocytes in the Spost C group increased;the rate of apoptosis decreased;the mitochondrial membrane potential of cardiomyocytes increased significantly;the m RNA expression level and protein of HIF-1α,Opa1 The expression level increased,the m RNA expression level and protein expression level of Drp1 decreased,but this change was reversed by the PI3 K specific inhibitor LY294002(P<0.05).Conclusion: Sevoflurane postconditioning can reduce myocardial ischemia-reperfusion injury by regulating mitochondrial OPA1 and drp1 through PI3 K / Akt pathway.