Attardi B, Fitzgerald T
Department of Medicine, Montefiore Hospital, Pittsburgh, Pennsylvania 15213.
Endocrinology. 1990 May;126(5):2281-7. doi: 10.1210/endo-126-5-2281.
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 less than 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 onset 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 less than 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 h of E2 treatment in the facilitation paradigm, serum inhibin was comparable (P greater than 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).(ABSTRACT TRUNCATED AT 400 WORDS)
本研究旨在利用先前建立的未成熟大鼠模型，研究孕酮对雌二醇（E2）诱导的促卵泡激素（FSH）激增及FSHβ信使核糖核酸（mRNA）的影响，该模型用于证明孕酮对促黄体生成素（LH）激增的抑制或促进作用。28日龄大鼠于09:00植入E2，在第29天（32小时后）约17:00出现FSH激增。单独用E2处理的大鼠此时血清FSH为15.1±1.6 ng/ml，而同时用E2和孕酮处理的动物血清FSH被显著抑制（8.3±0.7 ng/ml，P<0.001）。为证明孕酮的促进作用，在孕酮处理前先用E2对大鼠预处理24小时。这导致FSH分泌提前且增强：在第29天14:00，血清FSH为45.5±2.7 ng/ml，而单独用E2处理的大鼠为6.4±0.5 ng/ml。为研究孕酮的这些双重作用对FSH合成的影响，通过Northern分析测量FSHβ mRNA的稳态浓度。FSHβ mRNA通常与FSH释放平行增加。在经历E2诱导的FSH激增的大鼠中，该mRNA水平比激增被孕酮阻断的大鼠高约1.5倍。此外，在孕酮促进的FSH激增开始时，用E2和孕酮处理的动物中FSHβ mRNA比仅用E2处理的动物高约5倍。在FSH激增后的早晨（E2处理后48小时），FSHβ mRNA很低或无法检测到。相比之下，在激增被孕酮阻断的大鼠中此时FSHβ mRNA水平高7至8倍。单独用E2处理32小时（3077±260 fmol/ml）或48小时（2344±148 fmol/ml）的动物血清抑制素浓度与在抑制模式下用E2和孕酮处理的动物（分别为2469±106、1896±114 fmol/ml）相比显著升高（P<0.05）。在促进模式下E2处理32小时后，用空白植入物处理8小时的大鼠（2592±168 fmol/ml）和用孕酮处理8小时的大鼠（2720±188 fmol/ml）血清抑制素相当（P>0.2）。（摘要截短至400字）
