中文摘要：

目的：探讨血红素加氧酶-1（HO-1）对H9c2心肌细胞氧化应激损伤的保护作用及其作用机制。方法：建立过氧化氢（H2O2）诱导的H9c2心肌细胞氧化应激损伤模型,给予HO-1诱导剂氯化血红素（Hemin）预处理,或给予HO-1抑制剂锌原卟啉（Znpp-IX）共孵育。双波长法检测HO-1活性;四甲基偶氮唑盐（MTT）法检测细胞存活率;Hoechst33342染色和Caspase-3活性检测评估细胞凋亡;硫代巴比妥酸显色法检测丙二醛（MDA）含量,氮蓝四唑显色法检测总超氧化物歧化酶（SOD）活性;Western Blot法检测NF-κB蛋白表达水平。结果：与H2O2组相比,Hemin显著增加细胞HO-1活性,且该作用能被Znpp-IX阻断。与H2O2组相比,HO-1活性增加能够显著下调细胞凋亡率和Caspase-3活性,降低细胞MDA含量,增加总SOD活性,且上述作用能被Znpp-IX逆转。此外,HO-1活性增加能够显著抑制H2O2诱导的NF-κB激活,且该作用能被Znpp-IX逆转。结论：Hemin诱导的HO-1活性增加可能通过抑制NF-κB激活,维持细胞氧化还原平衡状态,抑制H2O2诱导的H9c2心肌细胞氧化应激损伤。

英文摘要：

Objective： To explore the protective effect of heme oxygenase - 1 on oxidative stress injury of cardiac H9c2 cells and the mechanism. Methods： The models of oxidative stress injury of cardiac H9c2 cells induced by H202 were established, then the models were pretreated with heroin （ heine oxygenase - 1 inducer） or co - incubated with zinc protoporphyrin - IX （heme oxygenase - ! inhibitor） . Double - wavelength spectroscopy was used to detect the activity of heme oxygenase - 1 ; MTF method was used to detect the survival rate of cells; Hoechst 33342 staining and Caspase -3 detection method were used to evaluate cell apoptosis; thiobarbituric acid （TBA） method was used to detect the content of malondialdehyde （MDA）, nitroblue tetrazolium method was used to detect the activity of total superoxide dis- mutase （SOD） ; Western Blot was used to detect the expression level of NF - KB protein. Results： Compared with H202 group, hemin im- proved the activity of berne oxygenase - 1 in cells significantly, and the effect could be blocked by zinc protoporphyrin - IX. Compared with H202 group, the increase of heme oxygenase - 1 activity down - regulated the apoptosis rate and Caspase - 3 activity significantly, reduced the content of MDA, and increased total SOD activity, and the effects above - mentioned could be reversed by zinc protoporphyrin - IX. In addition, heine oxygenase - 1 activity could inhibited NF - KB activation induced by H202 significantly, and the effect could be reversed by zinc protoporphyrin - IX. Conclusion： The increase of heme oxygenase - 1 activity induced by hemin Can inhibit oxidative stress injury of cardiac H9c2 cells induced by H202 by inhibiting activation of NF- KB and maintaining balanced state of cell oxidation reduction.