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Journal of Southern Medical University ; (12): 1154-1156, 2008.
Article in Chinese | WPRIM | ID: wpr-270188

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the protective effects of estrogen on the mitochondria in human umbilical vascular endothelial cells (HUVECs).</p><p><b>METHODS</b>HUVECs were exposed to H2O2 at 250 micromol/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.</p><p><b>RESULTS</b>Compared to the blank control group, H2O2 caused a decrease in complex IV activity, intracellular ATP level, and the cell viability, but elevated intracellular ROS. E2 pretreatment of cells significantly attenuated these effects of H2O2 exposure. ICI182780 administered prior to E2 pretreatment antagonized the protective effects of E2 against H2O2 exposure.</p><p><b>CONCLUSION</b>E2 offers mitochondrial protective effects on HUVECs, which is mediated by the estrogen receptors.</p>


Subject(s)
Female , Humans , Pregnancy , Cells, Cultured , Cytoprotection , Electron Transport Complex IV , Metabolism , Endothelial Cells , Cell Biology , Metabolism , Estrogens , Pharmacology , Hydrogen Peroxide , Pharmacology , Mitochondria , Metabolism , Oxidative Stress , Reactive Oxygen Species , Metabolism , Umbilical Veins , Cell Biology
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