Experimental study on miR-140-3p alleviates hypoxia/reoxygenation-induced myocardial cell injury by regulating PI3K/Akt pathway
Objective:To investigate the effect of miR-140-3p on hypoxia/reoxygenation-induced myocar-dial cell reperfusion injury by targeting PI3K/Akt pathway.Methods:H9C2 cardiomyocytes derived from rats were subjected to hypoxia/reoxygenation to induce cell injury.MiR-140-3p mimics and their control (NC)were transfected into H9C2 cardiomyocytes,and H9C2 cells overexpressing miR-140-3p were treated with 10μmol/L LY294002.The cardiomyocytes were divided into 6 groups,named control group (CON group),H/R group (Mod-el group),Model+NC group,Model+miR-140-3p mimics group,Model+miR-140-3p mimics+LY294002 group,Model+LY294002 group.The relative expression of miR-140-3 p in each group was detected by fluorescence quantitative PCR (RT-PCR).The viability of cardiomyocytes in each group was detected by CCK-8 method.The apoptosis rate of cardiomyocytes in each group was detected by flow cytometry.The expression levels of phosphorylated phosphatidylinositol 3 kinase (p-PI3K),phosphorylated protein kinase B (p-Akt),Bax,Bcl-2,and cleared caspases-3 in each group were detected by Western blot.Results:Compared with the CON group,the expression level and cell viability of miR-140-3p,as well as the expression of Bcl-2,p-PI3K,and p-Akt proteins,were significantly reduced in the Model group (P<0.05),while the expression and apoptosis rate of Bax and Cleared caspases-3 proteins were significantly increased (P<0.05).Compared with the Model group,overexpression of miR-140-3p upregulated the expression level and cell viability of miR-140-3p,as well as Bcl-2,p-PI3K,and p-Akt proteins,while downregulated the expression and apoptosis rate of Bax and Cleared caspases-3 proteins,LY294002 could inhibit the expression of miR-140-3p,downregulate cell viability and Bcl-2,p-PI3K,p-Akt proteins,and upregulate the expression of Bax,Cleared caspases-3 pro-teins and apoptosis rate.Conclusion:MiR-140-3p can alleviate autophagy and apoptosis in hypoxia/reoxygen-ation cardiomyocytes by regulating the PI3K/Akt pathway,thereby alleviating myocardial injury.