To explore the effects of 17-methoxyl-7-hydroxyl-benzofuran chalcone (YLSC) on apoptosis and oxidative stress induced by hypoxia/reoxygenation in H9c2 cells and the possible mechanisms.Cells were cultured under oxygen and glucose deprivation for 12 h and then under recovery conditions for 24 h to stimulate myocardial hypoxia/reoxygenation injury.Apoptosis and oxidative stress related molecules,protein expressions of Nuclear-Nrf2 and HO-1were tested.Compared with the model group,the cell viability,levels of SOD and GSH-Px were increased significantly in YLSC groups while the apoptotic rate and levels of ROS,LDH and MDA were significantly reduced.Western blot showed that the protein expressions of Nuclear-Nrf2,HO-1 and Bcl-2 in YLSC group were higher,while the expressions of Cleaved caspase 3 and Bax were lower than that in model group.However,combination treatment with Nrf2 inhibitor significantly inhibit the effects of YLSC.YLSC can protect H9c2 cells against apoptosis and oxidative stress induced by hypoxia/reoxygenation,and its mechanism may be associated with the activation of Nrf2/ARE signaling pathway.