Das C, Catt K J
Lancet. 1987 Sep 12;2(8559):599-601. doi: 10.1016/s0140-6736(87)92988-6.
the antifertility effects of the potent antiprogestin RU 486 (mifepristone) during early pregnancy have been attributed to its blockade of progesterone receptors in the endometrium. Studies in cultured syncytiotrophoblasts have revealed an additional action of RU 486 at the placental level, where it impairs the production of human chorionic gonadotropin (hCG), human placental lactogen (hPL), and progesterone. RU 486 (10 nmol-10 mumol/l) attenuated the production of all three placental hormones, in a dose-related manner, and its effects on hCG and hPL were reversed by addition of exogenous progesterone. The specific inhibitory effects of RU 486 on placental hormone secretion indicate that its antifertility actions are attributable to competitive inhibition of progesterone action in the trophoblast as well as in the endometrium.
强效抗孕激素RU 486（米非司酮）在妊娠早期的抗生育作用归因于其对子宫内膜中孕激素受体的阻断。对培养的合体滋养层细胞的研究揭示了RU 486在胎盘水平的另一种作用，即它会损害人绒毛膜促性腺激素（hCG）、人胎盘催乳素（hPL）和孕激素的产生。RU 486（10纳摩尔至10微摩尔/升）以剂量相关的方式减弱了所有三种胎盘激素的产生，并且通过添加外源性孕激素可逆转其对hCG和hPL的作用。RU 486对胎盘激素分泌的特异性抑制作用表明，其抗生育作用归因于对滋养层和子宫内膜中孕激素作用的竞争性抑制。
