EFFECTS OF PROGESTERONE ON THE ESTRADIOL-INDUCED FOLLICLE-STIMULATING-HORMONE (FSH) SURGE AND FSH-BETA MESSENGER-RIBONUCLEIC-ACID IN THE RAT
EFFECTS OF PROGESTERONE ON THE ESTRADIOL-INDUCED FOLLICLE-STIMULATING-HORMONE (FSH) SURGE AND FSH-BETA MESSENGER-RIBONUCLEIC-ACID IN THE RAT
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DOI：
10.1210/endo-126-5-2281
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发表时间：
1990-05-01
期刊：
影响因子：
4.8
通讯作者：
FITZGERALD, T
中科院分区：
文献类型：
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作者：
ATTARDI, B;FITZGERALD, T
本研究旨在研究孕酮对雌二醇（E2）诱导的FSH峰和FSH β的影响。信使RNA（mRNA）使用未成熟的大鼠模型，以前开发证明抑制或促进LH峰的孕酮。在0900 h接受E2植入的28日龄大鼠在第29天（32 h）约1700 h出现FSH激增。在仅用E2处理的大鼠中，血清FSH为15.1 ± 0.01。1.6 ng/ml，而在同时用E2和孕酮处理的那些动物中，血清FSH被显著抑制（8.3 ± 0.01）。0.7 ng/ml，P < 0.001）。为了证明孕酮促进作用，在孕酮处理之前，用E2对大鼠致敏24小时。这导致FSH分泌过早和增强：在第29天1400小时，血清FSH为45.5 ±-。2.7 ng/ml与6.4 .+-相比。0.5 ng/ml。为了检验孕酮的这些双重作用对FSH合成的影响，FSH β的稳态浓度为0.0001 μ mol/L。通过北方分析测定mRNA。FSH.beta. mRNA的增加通常与FSH的释放平行。这种mRNA的水平约1.5倍高，在大鼠经历E2诱导的FSH激增比大鼠中的激增被孕酮阻断。此外，在孕酮促进的FSH激增开始时，FSH β。mRNA是约5倍高，在与E2和孕酮治疗的动物比那些只与E2治疗。在FSH激增后的早晨（E2处理后48小时），FSH β。mRNA低至不可检测。相比之下，FSH β的水平。此时，在孕酮阻断峰的大鼠中，mRNA高出7至8倍。在单独用E2处理32小时的动物中，血清白蛋白浓度显著升高（P < 0.05）（3077 ± 0.05）。260 fmol/ml）或48 h（2344 . 148 fmol/ml）与在抑制范例中用E2和孕酮处理的那些相比（2469 . 106，1896 .+-. 114 fmol/ml）。在易化范例中，在32个E2处理后，在用空白植入物处理8小时的大鼠中，血清白蛋白是相当的（P > 0.2）（2592 ± 0.01）。168 fmol/ml）和用孕酮处理8小时的那些（2720 . ±. 188 fmol/ml）。总之，1）FSH激增伴随着FSH β的增加。mRNA的显著降低; 2）FSH β的显著降低。在激增大鼠中48小时的mRNA可能是由于在促性腺激素激增时升高的促性腺激素释放激素水平和/或增加的促性腺激素释放激素分泌，如我们先前所示，促性腺激素释放激素和促性腺激素释放激素两者都下调FSH β。原代培养大鼠垂体细胞mRNA水平。
This study was designed to investigate the effects of progesterone on the estradiol (E2)-induced FSH surge and FSH.beta. messenger RNA (mRNA) using immature rat models developed previously to demonstrate inhibition or facilitation of the LH surge by progesterone. Twenty-eight day-old rats that received E2 implants at 0900 h had FSH surges about 1700 h on day 29 (32 h). In rats treated with E2 alone, serum FSH was 15.1 .+-. 1.6 ng/ml at this time, while in those animals treated concurrently with E2 and progesterone, serum FSH was significantly suppressed (8.3 .+-. 0.7 ng/ml, P < 0.001). For demonstration of progesterone facilitation, rats were primed for 24 h with E2 before progesterone treatment. This led to premature and enhanced FSH secretion: at 1400 h on day 29 serum FSH was 45.5 .+-. 2.7 ng/ml compared to 6.4 .+-. 0.5 ng/ml in rats treated with E2 alone. To examine the effects of these dual actions of progesterone on FSH synthesis, steady state concentrations of FSH.beta. mRNA were measured by Northern analysis. FSH.beta. mRNA generally increased in parallel with FSH release. Levels of this mRNA were about 1.5-fold higher in rats undergoing E2-induced FSH surges than in rats in which the surge was blocked by progesterone. Also, at the outset of the progesterone-facilitated FSH surge, FSH.beta. mRNA was about 5-fold higher in animals treated with E2 and progesterone than in those treated with E2 only. On the morning after the FSH surge (48 h after E2 treatment) FSH.beta. mRNA was low to undetectable. In contrast, levels of FSH.beta. mRNA were 7- to 8-fold higher at this time in rats in which the surge was blocked by progesterone. Serum inhibin concentrations were significantly elevated (P < 0.05) in animals treated with E2 alone for 32 h (3077 .+-. 260 fmol/ml) or 48 h (2344 .+-. 148 fmol/ml) compared to those treated with E2 and progesterone in the inhibition paradigm (2469 .+-. 106, 1896 .+-. 114 fmol/ml, respectively). After 32 of E2 treatment in the facilitation paradigm, serum inhibin was comparable (P > 0.2) in rats treated for 8 h with blank implants (2592 .+-. 168 fmol/ml) and those treated for 8 h with progesterone (2720 .+-. 188 fmol/ml). In summary, 1)FSH surges are accompanied by increases in FSH.beta. mRNA in these models; 2) the profound decrease in FSH.beta. mRNA at 48 h in surging rats may be due to elevated inhibin levels and/or to increased GnRH secretion at the time of the gonadotropin surge as we showed previously that both inhibin and GnRH down-regulate FSH.beta. mRNA levels in primary cultures of rat pituitary cells.