THE EFFECT OF LHRH-A ON HCG AND PROGESTERONE BY HUMAN PLACENTA IN VITRO
SECRETION
Zhou Mei-hua, Chu Yun-hong, Zhu Bao-ting and Han Gui-zheng Department of Pharmacology,
Shanghai Medical University, Shanghai 200032, China
In this study, the effects of LHRH-A on the HCG and progesterone secretion of human placental tissues of different gestational ages; placental tissues from women receiving oral administration of tamoxifen; and placental tissue from early pregnant women in the presence of tamoxifen were observed. The results are as follows: (a) In the placental tissues from early gestation of 10 to 12 weeks, LHRH-A could stimulate HCG secretion, but had an obvious inhibitory effect on progesterone secretion. Since the placenta has been demonstrated to contain endogenous LHRH-like peptide, it is suggested that the endogenous LHRH-like peptide might exert a regulatory effect on placental HCG and progesterone secretion at different gestational ages. (b) In the present study, the placental villous cells from the early pregnant woman of 6 to 7 week gestation with or without oral administration of tamoxifen were cultured in vitro. The results showed that the response of placental villous cells from the tamoxifen treated women to LHRH-A was lower than those from untreated women. (c) The placental villous tissues from the pregnant woman of 6 to 7 week gestation were cultured in vitro in the presence or absence of tamoxifen. The results showed that the response of placental villous tissues to LHRH-A in the presence of tamoxifen was also lower than that in the absence of tamoxifen. From the results, it was clear that the effects of LHRH-A on the placental villous tissues treated by exogenous addition or oral administration of tamoxifen were lower than that on untreated villous tissues. It is therefore suggested that the endogenous LHRH-like peptide might take part in the inhibitory effect of tamoxifen on the secretion of placental villous tissues, which might be the reason why tamoxifen could potentiate the early pregnancy terminating effect of 15methyl-prostaglandin F2a.