Abstract:Objective To investigate the effects of wogonoside (Wog) on anoxiareoxygenation induced H9c2 myocardial cells injury and expression of P38 and ERK1/2.Methods H9c2 myocardial cells were cultured to construct anoxia/reoxygenation (A/R)model. They were given low, medium and high doses of Wog (12.5μM, 25μM, 50 μM) for 24h, respectively. Cell viability after 48h was detected by CCK8.Hochest staining was performed to detect apoptosis, ELISA was performed to detect contents ofmyocardial damage markers [creatine kinase (CK), creatine kinase isoenzyme (CK-MB),myoglobin (Mb)], and inflammatory cytokines [interleukin 6 (IL-6), interleukin 1β (IL-1β) and inducible nitric oxide synthase (iNOS)] in supernate. The kits were performed to detect contents of oxidative stress indexes [superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH)]. Western blot was performed to detect the expression of apoptosisrelated genes [Bcell lymphoma2(Bcl-2),Bcl2Associated X (Bax), Cysteinyl aspartate specific proteinase-3 (caspase-3), Caspase-9], mitogenactivated protein kinase P38 and extracellular regulated protein kinases (ERK1/2). Results The low, medium and high doses of Wog was performed to process A/R model cell H9c2, the cell survival rate, Bcl2 and expression of SOD were significantly increased, while apoptosis rate, Bax, Caspase-3, Caspase-9, CK, CK-MB, Mb, IL-6, I-1β, iNOS, MDA, LDH, P38 and ERK1/2 expression were significantly decreased (P<0.05).Conclusion Wog can reduce cardiomyocyte apoptosis by improving inflammatory reactions and oxidative stress damage. There are certain protective effects of Wogon A/R induced H9c2 myocardial cells injury, which may be related to downregulating phosphorylation of P38 and ERK1/2.