Massicotte J, Lachance R, Labrie F
J Steroid Biochem. 1984 Dec;21(6):745-54. doi: 10.1016/0022-4731(84)90040-2.
It is now well recognized that hCG-induced luteolysis is associated with hCG-induced desensitization, but the physiological significance of luteal cell GnRH, PGS and beta-receptors is still undefined. Therefore, we intend in this study to observe the effects of prostaglandin F2 alpha and prostaglandin E2 and the interactions between epinephrine, a potent LHRH agonist [(D-Ser-(TBu)6, des-Gly-NH2(10)) LHRH ethylamide: Buserelin] and hCG in normal and in vitro hCG-desensitized rat immature luteal cells in monolayer culture, on basal, hCG or cholera toxin stimulated intracellular and extracellular cyclic AMP and progesterone secretion. The present report shows that incubation of immature rat luteal cells in monolayer culture with Buserelin, led to 25-50% inhibition of the epinephrine--as well as PGE2--induced cyclic AMP and progesterone responses. The LHRH agonist can also reverse the stimulatory effects of cholera toxin in the presence of hCG and led with PGF2 alpha, to additive inhibitory effects on extracellular cyclic AMP accumulation induced by cholera toxin. Both Buserelin and PGF2 alpha can reverse the hCG-induced cyclic AMP and progesterone release but no effect could be observed when the incubation was carried out with either substance in the absence of hCG. Prostaglandin E2, in acute conditions of incubation, seems to share agonist properties with hCG when both were incubated with luteal cells. Buserelin reversed the stimulatory effects of PGE2, hCG, epinephrine, and cholera toxin on cyclic AMP and progesterone responses to these substances. These results suggest that Buserelin and PGF2 alpha have luteolytic-like effects and that there may be a complementary action for the two substances. Preincubation of rat luteal cells in monolayer culture with 1 nM hCG for a 24 h period led to the inhibition of cyclic AMP and progesterone responses after a subsequent exposure to hCG and epinephrine. Luteal cells were no longer responsive to hCG while the presence of epinephrine in hCG-desensitized cells led to a 40% stimulation of cAMP and progesterone production. These observations suggest that there occurred a partial alteration of the N component activity of the adenylyl cyclase system.
现已充分认识到，人绒毛膜促性腺激素（hCG）诱导的黄体溶解与hCG诱导的脱敏作用有关，但黄体细胞促性腺激素释放激素（GnRH）、前列腺素（PGS）和β受体的生理意义仍不明确。因此，在本研究中，我们打算观察前列腺素F2α和前列腺素E2以及肾上腺素、一种强效促黄体生成素释放激素（LHRH）激动剂[（D-丝氨酸-（叔丁基）6，去甘氨酸-NH2（10））LHRH乙酰胺：布舍瑞林]与hCG在单层培养的正常和体外hCG脱敏大鼠未成熟黄体细胞中的相互作用，对基础状态、hCG或霍乱毒素刺激的细胞内和细胞外环磷酸腺苷（cAMP）及孕酮分泌的影响。本报告显示，在单层培养中将未成熟大鼠黄体细胞与布舍瑞林一起孵育，导致肾上腺素以及前列腺素E2诱导的cAMP和孕酮反应受到25%-50%的抑制。在hCG存在的情况下，LHRH激动剂还可逆转霍乱毒素的刺激作用，并与前列腺素F2α一起，对霍乱毒素诱导的细胞外环磷酸腺苷积累产生相加抑制作用。布舍瑞林和前列腺素F2α均可逆转hCG诱导的cAMP和孕酮释放，但在无hCG的情况下用任何一种物质进行孵育时均未观察到效果。在急性孵育条件下，当前列腺素E2和hCG与黄体细胞一起孵育时，前列腺素E2似乎与hCG具有类似激动剂的特性。布舍瑞林逆转了前列腺素E2、hCG、肾上腺素和霍乱毒素对cAMP和孕酮对这些物质反应的刺激作用。这些结果表明，布舍瑞林和前列腺素F2α具有类似黄体溶解的作用，且这两种物质之间可能存在互补作用。在单层培养中将大鼠黄体细胞用1 nM hCG预孵育24小时，随后再暴露于hCG和肾上腺素后，会导致cAMP和孕酮反应受到抑制。黄体细胞对hCG不再有反应，而在hCG脱敏细胞中存在肾上腺素会导致cAMP和孕酮产生受到40%的刺激。这些观察结果表明，腺苷酸环化酶系统的N组分活性发生了部分改变。
