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作 者:陈国栋[1] 吴赛珠[1] 阮云军[1] 彭慧茹[1] 邢晓雯[1] 银孟卓[1] 简政威[1] 王玉筵[1]
机构地区:[1]南方医科大学南方医院心内科,广东广州510515
出 处:《南方医科大学学报》2008年第7期1154-1156,共3页Journal of Southern Medical University
基 金:国家重点基础研究发展计划(973计划)(2007CB507404)~~
摘 要:目的探讨雌激素对人脐静脉内皮细胞(HUVEC)线粒体的保护作用。方法采用过氧化氢(H2O2)作用于HUVEC制备氧化应激细胞模型,观察17β-雌二醇(E2)对氧化应激内皮细胞线粒体的保护作用。实验分A组(空白组)、B组(250 μmol/L H2O2刺激组)、C组(250 μmol/L H2O2+0.1 μmol/L E2组)及D组(250 μmol/L H2O2+0.1 μmol/L E2+10 μmol/L ICI182780组)。刺激4h后,检测细胞线粒体细胞色素C氧化酶活性、细胞内ATP水平、细胞内活性氧(ROS)水平及细胞活力。结果与A组比较,B组细胞中线粒体细胞色素C氧化酶活性下降,ATP水平下降,细胞内活性氧增加,细胞活力下降;C组细胞上述指标与B组细胞相比程度减轻;D组细胞上述指标与B组细胞变化相似。结论E2可通过受体机制对氧化应激HUVEC的线粒体产生保护作用。Objective To investigate the protective effects of estrogen on the mitochondria in human umbilical vascular endothelial cells (HUVECs). Methods HUVECs were exposed to H202 at 250 μmol/L for 4 h with or without pretreatment with 17-estradiol (E2) and ICI182780. Complex IV activity of the cells was measured with chromometry, and 2, 7-dichlorofluorescein diacetate (DCFH-DA) was used to determine intracellular reactive oxygen species (ROS). Intracellular adenosine triphosphate (ATP) level was quantified with a luciferin- and luciferase-based assay. Results Compared to the blank control group, H2O2 caused a decrease in complex Ⅳ activity, intracellular ATP level, and the cell viability, but elevated intracellularROS. E2 pretreatment of cells significantly attenuated these effects of H2O2 exposure. ICI182780administered prior to E2 pretreatment antagonized the protective effects of E2 against H2O2 exposure. Conclusion E2 offers mitochondrial protective effects on HUVECs, which is mediated by the estrogen receptors.
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