玉郎伞查尔酮激活Nrf2/ARE信号通路减轻缺氧/复氧所致的H9c2细胞凋亡及氧化应激损伤

17-Methoxyl-7-hydroxyl-benzofuran chalcone activates Nrf2/ARE pathway to protect H9c2 cells against apoptosis and oxidative stress induced by hypoxia/reoxygenation

研究玉郎伞查尔酮(YLSC)对缺氧/复氧所致的H9c2细胞损伤的影响及可能的作用机制。缺氧12 h、复氧24 h建立心肌细胞缺氧/复氧模型,并对细胞凋亡、氧化应激相关指标和Nuclear-Nrf2等蛋白表达进行了检测。结果显示,YLSC可明显增加细胞生存率,提高SOD、GSH-Px水平,降低细胞凋亡率和LDH、ROS、MDA水平。使Nuclear-Nrf2、HO-1、Bcl-2蛋白表达增高而Cleaved caspase 3、Bax蛋白表达减少,联合应用Nrf2抑制剂可抑制YLSC作用效果。结果表明,YLSC可以减轻缺氧/复氧所致的心肌细胞凋亡及氧化应激损伤,其机制可能与激活Nrf2/ARE信号通路有关。

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.