期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：14
页码：5129-5134
DOI：10.1073/pnas.0306720101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Other isotype-selective estrogen receptor (ER) agonists, the selective ER{alpha} agonist 3,17-dihydroxy-19-nor-17{alpha}-pregna-1,3,5 (10)triene-21,16{alpha}-lactone and the selective ER{beta} agonist 8-vinylestra-1,3,5 (10)-triene-3,17{beta}-diol, were used in hypophysectomized rats, gonadotropin-releasing hormone antagonist-treated mice, as well as intact rats to elucidate the effects of isotype-selective estrogens on the physiology of folliculogenesis and ovulation. In hypophysectomized rats and gonadotropin-releasing hormone antagonist-treated mice, the ER{beta} agonist caused stimulation of early folliculogenesis, a decrease in follicular atresia, induction of ovarian gene expression, and stimulation of late follicular growth, accompanied by an increase in the number of ovulated oocytes similar to 17{beta}-estradiol (E2). In contrast, the ER{alpha} agonist had little or no effect on these parameters, implying that direct estrogen effects on ovarian follicular development are mediated by ER{beta}. In intact rats, E2 and the ER{alpha} agonist dose-dependently inhibited ovulation, in contrast to the ER{beta} agonist. On the other hand, the ER{beta} agonist did not stimulate uterine weight in intact rats, in contrast to E2 and the ER{alpha} agonist. This finding is in line with the assumption that estrogen mediated ovulation inhibition and stimulation of uterine growth are mediated by ER{alpha} but not by ER{beta}
