【摘要】 目的:观察富含氢气（H₂）的培养基对血清-葡萄糖剥夺（SGD）致心肌细胞损伤的保护效应,探讨血红素加氧酶1（HO-1）在其中的作用。方法:用SGD的方法处理H9c2心肌细胞,建立缺血性心肌病的细胞模型。在SGD处理后,分别给予正常培养基和富含H₂的培养基以观察H₂的心肌细胞保护作用,给予选择性HO-1抑制剂锌原卟啉IX（ZnPP IX）以抑制HO-1的作用;各处理因素完成后,检测细胞存活率、羟基自由基（OH·）的含量及HO-1蛋白的表达。结果:SGD处理6³0 h,时间依赖性地降低H9c2心肌细胞的存活率,相关性分析显示r为-0.94。SGD处理6 h后再正常培养24 h可明显增加细胞内OH·的含量,并上调HO-1蛋白的表达,与对照组比较,均P<0.01。ZnPP IX通过抑制HO-1的作用能明显加重SGD处理诱导的心肌细胞存活率降低（P<0.05）。在SGD处理后给予富含H₂的培养基能减轻SGD引起的细胞损伤,使细胞存活率明显提高（P<0.05）,胞内OH·的含量显著降低（P<0.01）。富含H₂的培养基还能使SGD诱导的HO-1表达进一步上调,而ZnPPⅨ部分取消了H₂诱导的细胞保护作用（P<0.05）。结论:富含H₂的培养基可减轻血清-葡萄糖剥夺引起的心肌细胞损伤,其机制不仅与直接清除OH·有关而且还与上调抗氧化酶系统HO-1的表达有关。更多还原

【Abstract】 Objective:To investigate the protection of hydrogen gas（H₂）-rich medium from serum and glucose deprivation（SGD）-induced cardiac injury and the roles of heme oxygenase 1（HO-1）.Methods;The H9c2 cardiomyocytes（H9c2 cells） were treated with SGD to construct an in vitro model of ischemic cardiomyocyte injury.H9c2 cells were subsequently incubated in conventional and H₂- rich medium for measurement of the protective effects.Zinc protoporphyrin（ZnPP IX）,a selective HO-1 inhibitor,was employed to block the effects of HO-1.This was followed by measurement of cell viability,the level of hydroxyl free radical and HO-1 protein expression.Results;Treatment of H9c2 cells with SGD for 6 to 30 h timedependently attenuated the cell viability,as suggested by the correlation coefficient（r） of-0.94.Treatment with SGD for 6 h followed by 24 h incubation substantially augmented the content of hydroxyl free radical and HO-1expression compared with normal control group（both P <0.01）.Inhibition of HO-1 with ZnPP IX significantly aggravated SGD-induced cell damage in H9c2 cells（P <0.05）.H₂-rich medium following treatment with SGD markedly ameliorated the SGD-triggered cell injury leading to increased cell viability（P < 0.05） and reduced level of hydroxyl free radical（P <0.01）.H₂-rich medium also promoted the up-regulation of HO-1 induced by SGD,whilst inhibition of HO-1 with ZnPP IX partially abrogated the H₂-triggered cell protection effects（both P< 0.05）.Conclusion;H₂-rich medium ameliorates SGD-induced cardiomyocyte injury,the mechanisms of which may be associated with the elimination of hydroxyl free radical and up-regulation of HO-1.更多还原