Inhibition of salmon calcitonin on secretion of progesterone and GnRH-stimulated pituitary luteinizing hormone.
Inhibition of salmon calcitonin on secretion of progesterone and GnRH-stimulated pituitary luteinizing hormone.
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鲑鱼降钙素对黄体酮和 GnRH 刺激的垂体黄体生成素分泌的抑制作用。
DOI：
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Paulus S. Wang
中科院分区：
文献类型：
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作者：
S. Tsai;Chien‐Chen Lu;Jiann‐Jong Chen;Y. Chiao;Shyi;J. Hwang;Paulus S. Wang
本文研究了鲑鱼降钙素（sCT）对雌性大鼠孕酮生成和黄体生成素（LH）分泌的影响。给发情大鼠静脉注射生理盐水、sCT、人绒毛膜促性腺激素（hCG）或hCG + sCT。切除卵巢（Ovx）大鼠注射生理盐水或sCT。在体外实验中，颗粒细胞和垂体前腺（APs）与所试药物孵育。注射sCT可降低Ovx大鼠血浆LH水平。在体内和体外给予sCT可减少基础孕酮和hcg刺激的孕酮释放。8-溴- camp剂量依赖性地增加孕酮的产生，但不改变sCT的抑制作用。H-89不增强sCT的抑制作用。高剂量的25-羟基胆固醇和孕烯醇酮刺激孕酮的产生并减弱sCT的抑制作用。sCT不减少黄体生成素的基础释放，但预处理sCT减少促性腺激素释放激素（GnRH）刺激的黄体生成素分泌。这些结果表明，sCT通过阻止GnRH对大鼠APs中LH释放的刺激作用，并直接作用于卵巢颗粒细胞，降低camp后通路和类固醇生成酶的活性，从而抑制大鼠黄体酮的产生。
The effects of salmon calcitonin (sCT) on the production of progesterone and secretion of luteinizing hormone (LH) were examined in female rats. Diestrous rats were intravenously injected with saline, sCT, human chorionic gonadotropin (hCG), or hCG plus sCT. Ovariectomized (Ovx) rats were injected with saline or sCT. In the in vitro experiments, granulosa cells and anterior pituitary glands (APs) were incubated with the tested drugs. Plasma LH levels of Ovx rats were reduced by sCT injection. Administration of sCT decreased the basal and hCG-stimulated progesterone release in vivo and in vitro. 8-Bromo-cAMP dose dependently increased progesterone production but did not alter the inhibitory effect of sCT. H-89 did not potentiate the inhibitory effect of sCT. Higher doses of 25-hydroxycholesterol and pregnenolone stimulated progesterone production and diminished the inhibitory effects of sCT. sCT did not decrease basal release of LH by APs, but pretreatment of sCT decreased gonadotropin-releasing hormone (GnRH)-stimulated LH secretion. These results suggested that sCT inhibits progesterone production in rats by preventing the stimulatory effect of GnRH on LH release in rat APs and acting directly on ovarian granulosa cells to decrease the activities of post-cAMP pathway and steroidogenic enzymes.
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