Objective To investigate the effect and mechanism of engeletin on hypoxia reoxygenation injury in H9c2 cells.Methods A hypoxia reoxygenation model of H9c2 cells was constructed,and H9c2 cells were randomly divided into normoxia+vehicle group,normoxia+engeletin group,hypoxia reoxygenation+vehicle group,and hypoxia reoxygenation+engeletin group.Real-time quantitative polymerase chain reaction detection of mRNA levels of related antioxidant enzymes(peroxidase 2,glutathione peroxidase 1,catalase).The kit detects levels of superoxide dismutase,myocardial injury markers,malondialdehyde,and caspase-3.Immunohistochemical staining was used to detect cellular oxidative stress levels.TdT-mediated dUTP-biotin nick end labeling assay staining was used to detect the level of cell apoptosis.Western blot was used to detect the expression levels of red blood cell nuclear factor 2 related factor 2(Nrf2)and heme oxygenase 1(HO-1)related proteins.Results There was no statistically significant difference in myocardial injury markers,oxidative stress,cell apoptosis,and Nrf2,HO-1 protein expression between the normoxia+vehicle group and the normoxia+engeletin group(P＞0.05).Compared with the normoxia+vehicle group,the hypoxia reoxygenation+vehicle group showed a significant increase in myocardial injury markers,reactive oxygen species,malondialdehyde,cell apoptosis rate,and caspase-3 levels,while the mRNA levels of related antioxidant enzymes,superoxide dismutase levels,and Nrf2,HO-1 protein expression decreased significantly(P＜0.05).Compared with the hypoxia reoxygenation+vehicle group,the hypoxia reoxygenation+engeletin group showed a significant decrease in myocardial injury markers,reactive oxygen species,malondialdehyde,cell apoptosis rate,and caspase-3 levels.The mRNA levels of related antioxidant enzymes,superoxide dismutase levels,and Nrf2,HO-1 protein expression were significantly increased(P＜0.05).Conclusion Engeletin can alleviate oxidative stress damage and apoptosis in H9c2 cells subjected to hypoxia reoxygenation,possibly through the Nrf2/HO-1 pathway.
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