Morley P, Khalil M W, Calaresu F R, Armstrong D T
Department of Physiology, University of Western Ontario, London, Canada.
Biol Reprod. 1989 Sep;41(3):446-53. doi: 10.1095/biolreprod41.3.446.
It has been shown recently that catecholestrogens are produced by cultured porcine granulosa and thecal cells, and that they influence porcine granulosa cell steroidogenesis in a similar manner to estradiol-17 beta (E2). The present studies were performed to determine if catecholestrogens also play a role in the regulation of porcine thecal cell steroidogenesis and to compare their actions to those of E2. Thecal cells were obtained from prepubertal gilts and cultured in a serum-free medium for 48 h. Thecal cell androstenedione production under basal and luteinizing hormone (LH)-stimulated conditions was significantly inhibited by adding E2 or catecholestrogens to the culture medium. Treatment of basal and LH-stimulated cultures with increasing concentrations of E2 or catecholestrogens (0.1-10 micrograms/ml) caused a dose-and time-dependent inhibition of androstenedione production. The inhibitory effect of the catecholestrogens, but not of E2, was enhanced when the cultures contained the catechol-O-methyl transferase inhibitor, U-0521. Studies to determine the mechanism(s) of action of the catecholestrogens showed that E2 and catecholestrogen actions are exerted at a site(s) distal to cyclic adenosine 3'5' monophosphate (cyclic AMP) generation, because neither agent affected the basal or LH-stimulated accumulation of extracellular cyclic AMP, while causing a significant inhibition of androstenedione production. E2 or catecholestrogen treatment also inhibited androstenedione production stimulated by prostaglandin E2 and dibutyryl cyclic AMP. In addition, both E2 and catecholestrogen treatment significantly decreased basal and LH-stimulated 17 alpha-hydroxyprogesterone production, while significantly increasing pregnenolone production. Progesterone production in the presence of E2 or catecholestrogens showed small but statistically insignificant increases.(ABSTRACT TRUNCATED AT 250 WORDS)
最近研究表明，培养的猪颗粒细胞和卵泡膜细胞可产生儿茶酚雌激素，且它们对猪颗粒细胞类固醇生成的影响方式与雌二醇-17β（E2）相似。本研究旨在确定儿茶酚雌激素是否也在猪卵泡膜细胞类固醇生成的调节中发挥作用，并将它们的作用与E2的作用进行比较。从青春期前的小母猪获取卵泡膜细胞，并在无血清培养基中培养48小时。通过向培养基中添加E2或儿茶酚雌激素，基础条件下和促黄体生成素（LH）刺激条件下的卵泡膜细胞雄烯二酮生成受到显著抑制。用浓度递增的E2或儿茶酚雌激素（0.1 - 10微克/毫升）处理基础培养物和LH刺激的培养物，导致雄烯二酮生成呈剂量和时间依赖性抑制。当培养物中含有儿茶酚-O-甲基转移酶抑制剂U - 0521时，儿茶酚雌激素的抑制作用增强，而E2的抑制作用未增强。确定儿茶酚雌激素作用机制的研究表明，E2和儿茶酚雌激素的作用是在环磷酸腺苷（cAMP）生成的远端位点发挥的，因为这两种物质都不影响基础或LH刺激的细胞外环磷酸腺苷的积累，却能显著抑制雄烯二酮的生成。E2或儿茶酚雌激素处理也抑制了前列腺素E2和二丁酰环磷酸腺苷刺激的雄烯二酮生成。此外，E2和儿茶酚雌激素处理均显著降低基础和LH刺激的17α-羟孕酮生成，同时显著增加孕烯醇酮生成。在E2或儿茶酚雌激素存在下，孕酮生成有小幅增加，但在统计学上无显著意义。（摘要截短至250字）
