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前列腺素与小鼠排卵前卵泡成熟

Prostaglandins and preovulatory follicular maturation in mice.

作者信息

Downs S M, Longo F J

出版信息

J Exp Zool. 1983 Oct;228(1):99-108. doi: 10.1002/jez.1402280111.

Abstract

Experiments have been carried out in an effort to reverse the indomethacin-induced inhibition of preovulatory follicular development in immature superovulated mice utilizing prostaglandins E2 and F2 alpha. All mice were primed with 5 IU pregnant mare's serum gonadotropin followed 40 h later by 80 IU luteinizing hormone (LH). Animals were sacrificed 10 1/2 or 11 1/2-12 h post-LH, at which time ovaries were fixed and prepared for microscopic observation. Control mice receiving both indomethacin and prostaglandin (PG) vehicles averaged 92% germinal vesicle breakdown, and 82% of maturing oocytes were surrounded by an expanded cumulus oophorus. Ovarian weight increased by 29% and the apical walls of preovulatory follicles demonstrated appreciable thinning following LH administration. In mice receiving indomethacin plus PG vehicle, follicular maturation was suppressed in a dose-dependent manner; in mice receiving 10 mg/kg, less than 50% of the oocytes resumed meiosis and, of these, only 9% were accompanied by cumulus expansion. Ovarian weight gain was also inhibited, and the apical follicle wall exhibited few signs of preovulatory thinning. PGE2 and PGF2 alpha both reversed the inhibition of cumulus and oocyte maturation induced by indomethacin, though PGE2 was more effective. Only PGF2 alpha promoted apical follicular thinning, and neither PG had a significant effect on ovarian weight. We conclude that, in mice, PGs may play an integral role during preovulatory maturation of the oocyte and cumulus, as well as thinning of the apical wall.

摘要

利用前列腺素E2和F2α,开展了一系列实验,旨在逆转吲哚美辛对未成熟超排小鼠排卵前卵泡发育的抑制作用。所有小鼠均先用5国际单位孕马血清促性腺激素进行预处理,40小时后再注射80国际单位促黄体生成素(LH)。在注射LH后10.5或11.5 - 12小时处死动物,此时将卵巢固定并准备进行显微镜观察。接受吲哚美辛和前列腺素(PG)赋形剂的对照小鼠平均有92%的生发泡破裂,82%的成熟卵母细胞被扩张的卵丘包围。注射LH后,卵巢重量增加了29%,排卵前卵泡的顶壁明显变薄。在接受吲哚美辛加PG赋形剂的小鼠中,卵泡成熟受到剂量依赖性抑制;在接受10毫克/千克剂量的小鼠中,不到50%的卵母细胞恢复减数分裂,其中只有9%伴有卵丘扩张。卵巢重量增加也受到抑制,卵泡顶壁几乎没有排卵前变薄的迹象。PGE2和PGF2α均能逆转吲哚美辛诱导的卵丘和卵母细胞成熟抑制,尽管PGE2更有效。只有PGF2α能促进卵泡顶壁变薄,两种PG对卵巢重量均无显著影响。我们得出结论,在小鼠中,PGs可能在卵母细胞和卵丘的排卵前成熟以及顶壁变薄过程中发挥不可或缺的作用。

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