2-Methoxyestradiol Reduces Monocyte Adhesion to Aortic Endothelial Cells in Ovariectomized Rats

Endocrine Journal

Ryuzo KAWAMORI²  Tomoya MITA²  Satoru TAKEDA³  Hirotaka WATADA²  Kosuke AZUMA²  Yoshio FUJITANI²  Yukiko TOYOFUKU²  Kazuhisa IWABUCHI¹  Atsuko KUROKAWA³  Hideoki OGAWA¹  Takahisa HIROSE² 

[1] Institute for Environmental and Gender Specific Medicine, Juntendo University, School of Medicine;Departments of Medicine, Metabolism and Endocrinology, Juntendo University, School of Medicine;Department of Gynecology, Juntendo University, School of Medicine

关键词: Menopause;    Estrogen;    Hormone replacement therapy;    Cardiovascular disease;   

DOI  :  10.1507/endocrj.K07E-034

学科分类：内分泌与代谢学

来源: Japan Endocrine Society

【 摘 要 】

References(25)Cited-By(13)2-Methoxyestradiol (2-ME) is an endogenous metabolite of estradiol with no affinity for estrogen receptors. It inhibits cell proliferation, thus is a potentially useful drug to block the progression of atherosclerosis. As a first step to examining the anti-atherosclerotic effects of 2-ME, we investigated monocyte adhesion to aortic endothelial cells, which is considered a prerequisite to atherosclerosis in vivo. Eight-week-old Sprague-Dawley rats were ovariectomized then treated by slow-release pellets with placebo, 17-β-estradiol (5 μg/day), low-dose 2-ME (10 μg/day), or high-dose 2-ME (100 μg/day). After 6 weeks, enface analysis showed an increased number of monocytes adhering to endothelial cells of the thoracic aorta in ovariectomized rats compared with sham-operated controls. This increase was predominantly inhibited by treatment with 17β-estradiol, and low-dose or high-dose 2-ME. The observed effects were unrelated to changes in serum lipids, blood glucose, or blood pressure. Our data suggested that 2-ME mediates the anti-atherosclerotic actions of estradiol at least in part by preventing monocyte adhesion to the aortic endothelium.

【 授权许可】

Unknown