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哺乳动物中卵母细胞减数分裂、排卵和黄体化的激素调控。

Hormonal control of oocyte meiosis, ovulation and luteinization in mammals.

作者信息

Channing C P, Hillensjo T, Schaerf F W

出版信息

Clin Endocrinol Metab. 1978 Nov;7(3):601-24. doi: 10.1016/s0300-595x(78)80011-5.

Abstract

The ovulatory process can be regarded as a series of biochemical and morphological changes ultimately leading to the release of a mature oocyte and the transformation of the Graafian follicle into the corpus luteum. This process involves acute changes in steroidogenesis, resumption of oocyte meiosis, and finally rupture of the follicular wall and luteinization of the granulosa cells. Normally, all of these changes are induced synchronously by the pre-ovulatory LH surge. Experimentally, however, these changes in steroidogenesis, oocyte maturation and follicular rupture can be dissociated from each other showing that the LH effect is mediated via different cellular messengers. The gonadotrophins act in an orderly sequence to induce follicular maturation. The granulosa cells increase their number of LH receptors and respond to LH with increased stimulation of cyclic AMP accumulation and progesterone secretion. Concomitantly, they decrease in their FSH receptors and their response to FSH diminishes in terms of ability to stimulate cyclic AMP accumulation. The ovulatory process is associated with increased uptake of LH by the follicle; when granulosa cells are obtained from pre-ovulatory follicles and cultured they luteinize spontaneously. Steroid hormones modulate the actions of gonadotrophins on follicular maturation. In addition, there are non-steroidal factors in follicular fluid which regulate follicular maturation: an oocyte maturation inhibitor keeps the oocyte in meiotic arrest; a luteinizing inhibitor prevents the granulosa cells from luteinizing prior to follicular rupture; a folliculostatin inhibits FSH release from the pituitary gland. The functional activity and the lifespan of the corpus luteum depend on adequate pre-ovulatory as well as post-ovulatory gonadotrophic stimulation. Its lifespan may also be regulated by an LH binding inhibitor.

摘要

排卵过程可被视为一系列生化和形态学变化,最终导致成熟卵母细胞的释放以及格拉夫卵泡转化为黄体。这个过程涉及类固醇生成的急性变化、卵母细胞减数分裂的恢复,最终是卵泡壁的破裂和颗粒细胞的黄体化。正常情况下,所有这些变化都是由排卵前促黄体生成素(LH)峰同步诱导的。然而,在实验中,类固醇生成、卵母细胞成熟和卵泡破裂的这些变化可以相互分离,这表明LH的作用是通过不同的细胞信使介导的。促性腺激素按有序顺序起作用以诱导卵泡成熟。颗粒细胞增加其LH受体数量,并对LH作出反应,增加环磷酸腺苷(cAMP)积累和孕酮分泌的刺激。与此同时,它们的促卵泡生成素(FSH)受体减少,并且它们对FSH的反应在刺激cAMP积累的能力方面减弱。排卵过程与卵泡对LH摄取的增加有关;当从排卵前卵泡获得颗粒细胞并进行培养时,它们会自发黄体化。类固醇激素调节促性腺激素对卵泡成熟的作用。此外,卵泡液中存在非甾体因子调节卵泡成熟:一种卵母细胞成熟抑制剂使卵母细胞处于减数分裂停滞状态;一种黄体化抑制剂在卵泡破裂前阻止颗粒细胞黄体化;一种卵泡抑素抑制垂体释放FSH。黄体的功能活性和寿命取决于排卵前以及排卵后足够的促性腺激素刺激。其寿命也可能受LH结合抑制剂调节。

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