Objective To investigate the protective effects of oxyresveratrol(Oxy)on hypoxia/reoxygenation(H/R)-induced cardiac oxidative myocardial injury.Methods Mouse myocardial HL-1 cells were cultured in DMEM high-sugar complete medium as the control group(Ctrl group).HL-1 cells were subjected to 6 hours of hypoxia and 2 hours of reoxygenation to establish a myocardial H/R injury model(H/R group).Ctrl group cells were pre-incubated with 20 μM Oxy in DMEM complete medium for 2 hours before H/R stimulation(H/R+Oxy group).Cell viability was detected by cell counting kit-8 assay.Protein expression levels of B-cell lymphoma-2(Bcl-2),Bcl-2-associated X(Bax),and nuclear factor erythroid-2-related factor 2(Nrf-2)were detected by Western blot.Apoptosis in each group was evaluated using terminal uridine nucleotide end labeling(TUNEL)and Hoechst assay.The mRNA expression levels of Nrf-2,heme oxygenase-1(Ho-1),and quinone oxidoreductase 1(Nqo-1)were analyzed using real-time quantitative PCR.Superoxide dismutase(SOD)and malondialdehyde(MDA)levels in cells from each group were measured using corresponding assay kits and a microplate reader.Results Compared to the Ctrl group,the H/R group showed decreased cell viability,increased Bax protein level,decreased Bcl-2 protein level,elevated apoptosis,reduced SOD level,and increased MDA level,with statistically significant differences(P<0.05).Compared to the H/R group,the H/R+Oxy group exhibited increased cell viability,decreased Bax protein level,increased Bcl-2 protein level,reduced apoptosis,increased SOD level,decreased MDA level,and elevated mRNA expression of Nrf-2,Ho-1,and Nqo-1,with statistically significant differences(P<0.05).Conclusion Oxy can inhibit H/R-induced myocardial cell injury,and may play an antioxidant role by activating the Nrf-2 signaling pathway.
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