Resveratrol Protects Cardiomyocytes Against Anoxia/reoxygenation Injury By Promoting VDAC1 Deacetylated Modification

Objective: Resveratrol is a phytoalexin and a polyphenolic compound,it has very strong biological activities.Resveratrol has been a hotspot of research both in pharmacology and clinical medicine since it was discovered,there are growing evidence suggested that Resveratrol could have great significant for treatment and prevention cardiovascular diseases.In this study,We aim to explore the relationship of VDAC1 acetylated modification and SIRT1 protein when had used Resveratrol pretreatment on H9c2 cardiomyocytes against anoxia/reoxygenation(A/R)injury.Method: In this study,an in vitro I/R model was replicated on H9c2 cardiomyocytes by A/R treatment.SIRT1,VDAC1,acetyl-VDAC1,Cytochrome C(Cyt c),Bax and Bcl-2 protein expression was detected by Western Blotting and Immunoprecipitation.According to the kit,the activity of CPK,LDH,MDA,SOD and GSH-Px were measured by UV spectrophotometer.The levels of intracellular ROS,the mitochondrial membrane potential(??m)and the apoptosis were detected by flow cytometry.Results: 1.Preconditioning with Resveratrol,the expression of VDAC1,acetyl-VDAC1 and Bax protein expression were dropped compared with A/R group,the expression of SIRT1 and Bcl-2 protein were remarkably increased compared to A/R group(p<0.05).2.To compared with Resveratrol pretreatment group,When used the specific inhibitor of SIRT1(Ex527)would reduce VDAC1 deacetylated levels,the cell viability would remarkably decreased,the activity of CPK and LDH increased,cellular content of MDA increased,the content of SOD and GSH-Px was lower(p<0.01).3.While VDAC1 deacetylated modification were inhibited by Ex527,A/R injury would induced ROS generation,decreased the stability of mitochondrial membrane potential(??m),increased the release of cytochrome c from the mitochondria into cytosol and finally induced cell apoptosis(p<0.01).Conclusion: Resveratrol activates SIRT1 protein,prompts VDAC1 deacetylated modification,subsequently inhibit the mitochondrial apoptosis pathway,reduce cell apoptosis,finally protects cardiomyocytes against anoxia/reoxygenation injury.