| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1992628 | The Journal of Steroid Biochemistry and Molecular Biology | 2009 | 7 Pages |
ObjectiveThis study discussed the role of estrogen as an antioxidant in the damage of vascular endothelial cells.DesignWe treated bovine aortic endothelial cells (bAEC) either with 1 mM of H2O2 alone or with 1 μM of 17β-estradiol (E2) for 24 h followed by 1 mM of H2O2 for 3 h. The cell survival was evaluated by MTT assay, cellular apoptosis by fluorescence activated cell sorter (FACS) and Hoechst 33342 staining, oxidative stress by intracellular reactive oxygen species (ROS) and apoptosis after oxidative stress by western blotting for phospho-p38, p38, and Bcl-2.ResultsMTT assay showed that bAEC viability was reduced to 55.7 ± 3.0% and 39.1 ± 3.7% after 30 and 60 min of H2O2 treatment, respectively. E2 and H2O2 treated cells did not show significant decrease in the cell survival. Similarly the FACS analysis and Hoechst 33342 stain showed that the latter decreased cellular apoptosis induced by H2O2. Intracellular ROS increased by 181.6 ± 68.9% in the former and by 37.0 ± 3.9% in the latter (P < 0.05). The expression of phospho-p38 mitogen-activated protein kinase (MAPK) was higher in the latter.ConclusionsE2 mediates antioxidant effects on the oxidative stress induced by H2O2. This antioxidant effect on bAEC may elucidate the scientific basis of hormone therapy for maintaining cardiovascular integrity in postmenopausal women.
