【摘要】 目的 :研究黄芪甲苷（astragalosideⅣ,AS-Ⅳ）对过氧化氢（H₂O₂）诱导的人主动脉内皮细胞（human aortic endothelial cells,HAECs）氧化应激损伤的改善作用。方法 :体外培养的HAECs经饥饿处理后分为对照组、H₂O₂损伤组及AS-Ⅳ治疗组。H₂O₂损伤组细胞经H₂O₂（400μmol/L）持续损伤36 h,AS-Ⅳ治疗组细胞经H₂O₂损伤12 h后加入含50μg/m L AS-Ⅳ的培养基继续干预处理24 h。观察AS-Ⅳ对H₂O₂诱导的HAECs氧化应激损伤及线粒体功能损伤的修复作用。结果:H₂O₂损伤后HAECs丙二醛（MDA）含量、NADPH氧化酶活性及线粒体活性氧（ROS）水平显著增加,超氧化物歧化酶（SOD）和锰超氧化物歧化酶（Mn-SOD）活性及线粒体膜电位显著降低;H₂O₂损伤的HAECs经AS-IV治疗后,HAECs的MDA含量、NADPH氧化酶活性及线粒体ROS含量明显降低,SOD和Mn-SOD活性及线粒体膜电位显著增高。结论:AS-Ⅳ对H₂O₂诱导的HAECs氧化应激损伤具有保护作用,提高线粒体的抗氧化功能是其可能的机制之一。更多还原

【Abstract】 Objective: To investigate the beneficial effects of astragaloside IV（AS-Ⅳ） on oxidative stress injury induced by hydrogen peroxide（H₂O₂） in cultured human aortic endothelial cells（HAECs）. Methods: HAECs were cultured in vitro and randomly divided into Control group, H₂O₂ treated group,and AS-Ⅳ treated group. The cells were treated with H₂O₂（400 μmol/L） for 36 hours as H₂O₂ group. For AS-Ⅳ treatment, the cells were first treated with H₂O₂ for 12 hours, then AS-Ⅳ（50 μg/m L） were added into culture medium for 24 h. After 36 h, all the cells were examined for oxidative stress injury and mitochondrial antioxidative function. Results:Compared with the Control cells, the addition of H₂O₂ significantly increased the MDA content, NADPH oxidase activity, and mitochondrial ROS content of the cells, whereas the SOD activity, Mn-SOD activity and mitochondrial transmembrane potential level were significantly decreased. The administration of AS-Ⅳ significantly decreased NADPH oxidase activity, MDA content and mitochondrial ROS content, and increased SOD activity, Mn-SOD activity and mitochondrial transmembrane potential level, compared with those of H₂O₂ treated injured cells. Conclusion: In the present study, AS-Ⅳ attenuates H₂O₂ induced oxidative stress in HAECs. The enhancement of mitochondrial antioxidant function by AS-Ⅳ may be one of the possible pathways of AS-Ⅳ to protect HAECs from oxidative stress.更多还原