Synergistic effects of steroids with FSH on folliculogenesis, steroidogenesis and FSH- and hCG-receptors in hypophysectomized mice.
Synergistic effects of steroids with FSH on folliculogenesis, steroidogenesis and FSH- and hCG-receptors in hypophysectomized mice.
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DOI：
10.1530/jrf.0.0990403
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发表时间：
1993-11
期刊：
影响因子：
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通讯作者：
Xiaohong Wang;G. S. Greenwald
中科院分区：
文献类型：
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作者：
Xiaohong Wang;G. S. Greenwald
注射绵羊FSH（4 μ g/天）4天至垂体切除的小鼠，不能使卵泡生成恢复到正常的周期值。这可能是由于雌二醇的生产不足。本研究旨在确定FSH和LH诱导的雌二醇是否对各个阶段卵泡的生长和分化至关重要。垂体切除后12天，将小鼠皮下注射。每天给予10、50或250微克环戊基丙酸雌二醇，伴或不伴绵羊FSH（4微克/天）1-4天。每只动物的一个卵巢用于组织学检查。从第二个卵巢中分离不同阶段的卵泡，用[3 H]胸苷孵育3 h，以测定DNA合成速率。孵育培养基和血清用于类固醇测定。单独雌二醇治疗后，血清雌二醇呈剂量依赖性反应，但卵巢和子宫重量并没有随着雌二醇剂量的增加而进一步增加。这一发现与腔前卵泡和小腔卵泡数量增加一致，但不包括排卵前卵泡的发育。用10和50 μ g环戊基丙酸雌二醇治疗不能防止窦状卵泡发生闭锁。较高剂量（250微克天-1）的雌二醇环戊基丙酸酯延迟闭锁的窦卵泡，并保持更多的大健康的窦卵泡。在同时注射雌二醇和FSH后，卵巢重量是单独注射FSH或雌二醇的2-3倍;在所有发育阶段的卵泡数量和卵泡DNA合成增加，而没有任何闭锁的迹象;雌二醇的体外积累也增加。雌二醇单独诱导颗粒细胞中的FSH受体，但不诱导任何卵巢隔室中的hCG受体; FSH单独诱导颗粒细胞中的FSH和hCG受体，但不诱导卵泡膜间质组织中的FSH和hCG受体，而雌二醇加FSH增强颗粒细胞中的FSH受体和颗粒和卵泡膜间质组织中的LH/hCG受体。雌二醇与FSH的协同作用被相同剂量的己烯雌酚、睾酮或双氢睾酮模仿，但后者类固醇仅增加有腔卵泡的数量，可能是因为它们的半衰期较短。这些结果表明，在小鼠中，雌二醇刺激腔前和腔卵泡的生长，并延迟卵泡闭锁;雌激素和雄激素与FSH协同作用，以促进卵泡增殖和分化，并防止卵泡闭锁。
Injection of ovine FSH (4 micrograms day-1) for 4 days into hypophysectomized mice does not restore folliculogenesis to normal cyclic values. This may be due to insufficient production of oestradiol. The present study was designed to determine whether FSH- and LH-induced oestradiol was critical for growth and differentiation of follicles at all stages. Twelve days after hypophysectomy, mice were injected s.c. with 10, 50 or 250 micrograms oestradiol cyclopentylpropionate daily with or without ovine FSH (4 micrograms day-1) for 1-4 days. One ovary from each animal was used for histology. From the second ovary, follicles were isolated at different stages and incubated with [3H]thymidine for 3 h to determine the rate of DNA synthesis. Incubation medium and serum were used for steroid determinations. After oestradiol treatment alone, there was a dose-dependent response in serum oestradiol, but ovarian and uterine weights did not increase further with the increasing doses of oestradiol administered. This finding was consistent with an increase in the number of preantral follicles and small antral follicles but excluding the development of preovulatory follicles. Treatment with 10 and 50 micrograms of oestradiol cyclopentylpropionate did not prevent antral follicles from undergoing atresia. The higher dose (250 micrograms day-1) of oestradiol cyclopentylpropionate delayed atresia of antral follicles and maintained more large healthy antral follicles. After concurrent injection of oestradiol and FSH, ovarian weight was 2-3 times greater than with either FSH or oestradiol alone; the number of follicles and follicular DNA synthesis at all stages of development increased without any signs of atresia; the in vitro accumulation of oestradiol also increased. Oestradiol alone induced FSH receptors in granulosa cells, but did not induce hCG receptors in any ovarian compartment; FSH alone induced FSH and hCG receptors in granulosa cells but not in thecal-interstitial tissues, whereas, oestradiol plus FSH enhanced FSH receptors in granulosa cells and LH/hCG receptors in granulosa and thecal-interstitial tissues. The synergistic effect of oestradiol with FSH was mimicked by the same dose of diethylstilboestrol, testosterone or dihydrotestosterone, but the latter steroids increased only the number of antral follicles, presumably because of their shorter half-lives. These results indicate that in mice oestradiol stimulates the growth of preantral and antral follicles and delays follicular atresia; oestrogens and androgens act synergistically with FSH to enhance follicular proliferation and differentiation, and prevent follicles from undergoing atresia.