Protective effects of estrogen on mitochondria in human umbilical vascular endothelial cells.
- Author:
Guo-dong CHEN
1
;
Sai-zhu WU
;
Yuan-jun RUAN
;
Hui-ru PENG
;
Xiao-wen XING
;
Meng-zhuo YIN
;
Zheng-wei JIAN
;
Yu-yan WANG
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Cytoprotection; drug effects; Electron Transport Complex IV; metabolism; Endothelial Cells; cytology; drug effects; metabolism; Estrogens; pharmacology; Female; Humans; Hydrogen Peroxide; pharmacology; Mitochondria; drug effects; metabolism; Oxidative Stress; drug effects; Pregnancy; Reactive Oxygen Species; metabolism; Umbilical Veins; cytology
- From: Journal of Southern Medical University 2008;28(7):1154-1156
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of estrogen on the mitochondria in human umbilical vascular endothelial cells (HUVECs).
METHODSHUVECs 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.
RESULTSCompared 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.
CONCLUSIONE2 offers mitochondrial protective effects on HUVECs, which is mediated by the estrogen receptors.
