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目的比较木犀草素对物理性及化学性缺氧/复氧引发H9c2心肌细胞损伤的影响,考察木犀草素对抗两种缺氧/复氧损伤作用。方法体外培养H9c2心肌细胞,以N2饱和缺氧箱及Na2S2O4为缺氧环境分别建立缺氧/复氧损伤模型。测定H9c2心肌细胞存活率、乳酸脱氢酶漏出量、丙二醛的生成量、超氧化物歧化酶以及活性氧的生成量、线粒体膜电位(△Ψm)的变化,考察木犀草素对H9c2心肌细胞缺氧/复氧损伤的影响。结果与模型组比较,木犀草素能显著增强缺氧/复氧损伤心肌细胞存活率,抑制乳酸脱氢酶漏出、丙二醛和活性氧的生成量,提高超氧化物歧化酶的活性(P<0.05或P<0.01),恢复细胞膜电位水平。结论木犀草素对缺氧/复氧心肌细胞损伤有明显的保护作用,能够有效维持抗氧化防御机制与自由基之间的平衡。
Objective To compare the effects of luteolin on physical and chemical hypoxia / reoxygenation-induced cardiomyocyte injury in H9c2 cells and investigate the protective effect of luteolin against both hypoxia / reoxygenation injury. Methods H9c2 cardiomyocytes were cultured in vitro and hypoxia / reoxygenation injury models were established by hypoxia tank N2 and Na2S2O4 hypoxia respectively. The survival rate of H9c2 cardiomyocytes, the leakage of lactate dehydrogenase, the formation of malondialdehyde, the production of superoxide dismutase and reactive oxygen species, the mitochondrial membrane potential (△ ψm) were measured to investigate the effect of luteolin on H9c2 myocardium Effect of cell hypoxia / reoxygenation injury. Results Compared with the model group, luteolin could significantly enhance the survival rate of hypoxia / reoxygenation injury myocardial cells, inhibit lactate dehydrogenase leakage, malondialdehyde and reactive oxygen species generation, increase the activity of superoxide dismutase (P <0.05 or P <0.01), restore the cell membrane potential level. Conclusion Luteolin has a significant protective effect on hypoxia / reoxygenation cardiomyocyte injury, which can effectively maintain the balance between antioxidant defense mechanism and free radicals.