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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 effect of estrogen on mitochondria of human umbilical vein endothelial cells (HUVECs). Methods Hydrogen peroxide (H2O2) was used to produce oxidative stress cell model in HUVEC. The protective effect of 17β-estradiol (E2) on oxidative stress-induced endothelial cell mitochondria was observed. The experimental group A (blank group), B group (250 μmol / L H2O2 stimulation group), C group (250 μmol / L H2O2 + 0.1 μmol / L E2 group) and D group L E2 + 10 μmol / L ICI182780 group). After stimulated for 4h, mitochondrial cytochrome C oxidase activity, intracellular ATP level, intracellular reactive oxygen species (ROS) and cell viability were measured. Results Compared with group A, the activity of mitochondrial cytochrome C oxidase in group B decreased, the level of ATP decreased, the level of reactive oxygen species increased, and the viability of cells decreased in group B. The level of mitochondrial cytochrome C oxidase in group B decreased compared with that in group B; The above indicators and group B cells similar changes. Conclusion E2 can protect mitochondria of oxidative stress HUVEC through receptor mechanism.