OBJECTIVE: This study discussed the role of estrogen as an antioxidant in the damage of vascular endothelial cells. DESIGN: We treated bovine aortic endothelial cells (bAEC) either with 1mM of H(2)O(2) alone or with 1 microM of 17beta-estradiol (E(2)) for 24h followed by 1mM of H(2)O(2) for 3h. 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. RESULTS: MTT assay showed that bAEC viability was reduced to 55.7+/-3.0% and 39.1+/-3.7% after 30 and 60 min of H(2)O(2) treatment, respectively. E(2) and H(2)O(2) 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 H(2)O(2). 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. CONCLUSIONS: E(2) mediates antioxidant effects on the oxidative stress induced by H(2)O(2). This antioxidant effect on bAEC may elucidate the scientific basis of hormone therapy for maintaining cardiovascular integrity in postmenopausal women.
OBJECTIVE: This study discussed the role of estrogen as an antioxidant in the damage of vascular endothelial cells. DESIGN: We treated bovine aortic endothelial cells (bAEC) either with 1mM of H(2)O(2) alone or with 1 microM of 17beta-estradiol (E(2)) for 24h followed by 1mM of H(2)O(2) for 3h. 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. RESULTS:MTT assay showed that bAEC viability was reduced to 55.7+/-3.0% and 39.1+/-3.7% after 30 and 60 min of H(2)O(2) treatment, respectively. E(2) and H(2)O(2) 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 H(2)O(2). 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. CONCLUSIONS: E(2) mediates antioxidant effects on the oxidative stress induced by H(2)O(2). This antioxidant effect on bAEC may elucidate the scientific basis of hormone therapy for maintaining cardiovascular integrity in postmenopausal women.
Authors: Jue Lin; Candyce H Kroenke; Elissa Epel; Heather A Kenna; Owen M Wolkowitz; Elizabeth Blackburn; Natalie L Rasgon Journal: Brain Res Date: 2010-10-18 Impact factor: 3.252
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