Objective To investigate the effect of propofol postconditioning(P-PostC)on apoptosis and autophagy induced by ischemia/reoxygenation in H9c2 cardiomyocytes under high glucose environment.Method In Fengxian District Central Hospital of Shanghai in April 2023,Rat heart-derived H9c2 cells were exposed to high glucose for 48 h,and then subjected to hypoxia/reoxygenation(H/R)in the absence or presence of different concentrations of P-PostC postconditioning.The cells were divided into groups as:NC group,HG group,NC+H/R group,HG+H/R group,HG+H/R+P12.5 group,HG+H/R+P25 group,HG+H/R+P50 group,HG+H/R+P100 group and HG+H/R+P25+Brusatol group.After the concentration of propofol was determined,H/R and P-PostC treatments were performed on H9c2 cells with or without Nrf2/HO-1 pathway inhibitors to explore their role in the protection of apoptosis and autophagic cell death under P-PostC-mediated high glucose.Results The results showed that high glucose with or without H/R decreased the viability of H9c2 cells,increased the release of lactate dehydrogenase and the production of reactive oxygen species,all of which were significantly reversed by P-PostC,especially at 25 μmol/L(P25)concentration(P<0.05).In addition,it was found that propofol(P25)reduced the apoptosis and autophagy of H9c2 cells and increased the expression of Nrf2 and HO-1(P<0.05)meanwhile.The protective effect of propofol(P25)on H/R injury was reversed by using Nrf2/HO-1 pathway inhibitors(P<0.05).Conclusion P-PostC would reduce H/R-induced apoptosis and autophagy in H9c2 heart cells by up-regulating the activity of Nrf2/HO-1 pathway in the high glucose state.
维普
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