【摘要】 目的:观察木犀草素-7-O-β-D-葡萄糖苷对过氧化氢(H2O2)诱导乳鼠心肌细胞氧化损伤的作用及其机制。方法:木犀草素-7-O-β-D-葡萄糖苷预作用12 h后,采用H2O2诱导培养乳鼠心肌细胞氧化损伤模型,测定细胞存活率、细胞内超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量、细胞内活性氧(ROS)水平及细胞内钙(Ca2+)超载的变化。结果:木犀草素-7-O-β-D-葡萄糖苷能明显提高H2O2损伤细胞存活率,提高细胞内SOD活性,降低胞内MDA和ROS生成量,同时使细胞内钙含量降低。结论:木犀草素-7-O-β-D-葡萄糖苷对H2O2氧化损伤心肌细胞具有明显的保护作用,机制可能与其抑制脂质过氧化、抑制细胞内钙超载有关。更多还原

【Abstract】 Objective:To observe the effects of luteolin-7-O-β-D-glucopyranoside on neonatal rat cardiomyocytes injuried by hydrogen peroxide(H2O2)and study its mechanisms.Methods:After 12 hours′preconditioning of luteolin-7-O-β-D-glucopyranoside,the model of oxidative injury was induced by H2O2 in cultured neonatal rat cardiomyocytes.The viability of cardiomyocytes,superoxide dismutase(SOD)activities and intracellular malonaldehyde(MDA)levels and reactive oxygen species(ROS)activities and intracelluar calcium level were measured respectively.Results:In the model of oxidative injury induced by H2O2,preconditioning of luteolin-7-O-β-D-glucopyranoside could significantly raise the viability of cardiomyocytes and SOD activities,and decrease intracellular ROS and MDA generation,the intracelluar calcium level was decreased at the same time.Conclusion:Preconditioning of luteolin-7-O-β-D-glucopyranoside could obviously protect cultured neonatal rat cardiomyocytes from oxidative damages,and the beneficial effects may be re-lated to its antioxidant properties and reduce of intracelluar calcium overload.更多还原