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[细胞因子与黄体]

[Cytokines and the corpus luteum].

作者信息

Martal J, Chêne N, Huynh L, Gharib-Hamrouche N, de la Llosa-Hermier M P

机构信息

INRA, Station de physiologie animale, Unité d'endocrinologie de l'embryon, Jouy-en-Josas.

出版信息

Contracept Fertil Sex. 1994 Oct;22(10):635-47.

PMID:7804383
Abstract

This minireview present main findings concerning the contribution of cytokines to the regulation of some key processes of luteal functions. Data concerning the preovulatory follicles invasion by white blood cells and the migration of macrophages, granulocytes and T lymphocytes into corpus luteum suggest that local secretion of regulatory cytokines may be involved in regulating corpus luteum formation and demise as well its maintenance in early pregnancy. Several lines of evidence indicate that the pro-inflammatory cytokines such as IL-1, IL-6 and TNF-alpha modulate the steroidogenic changes which take place during luteinization. For instance, an inhibition of E2 biosynthesis is evidenced in granulosa cells in human or porcine species with IL-1, in rat with TNF-a and in bovine with IL-6. Moreover, IL-1 stimulates P4 production but to a much lower extent than LH, and PGE2 synthesis by rat thecal cells. The potential relevance of pro-inflammatory cytokines in the mechanisms controlling luteolysis is suggested by the ability of IL-1 and TNF-alpha to decrease both P4 production and the survival of bovine luteal cells. As opposed to ruminants, TNF-alpha has no effect in human luteal cells but potentiates the decrease of P4 secretion induced by IFN-gamma. Finally, data regarding the participation of trophoblast interferons in the mechanisms for maintaining the corpus luteum at the establishment of pregnancy are now available in ruminants. From these observations and others, we can consider that cytokines are involved in the regulation of the corpus luteum function.

摘要

本综述介绍了细胞因子对黄体功能某些关键过程调节作用的主要研究结果。有关白细胞对排卵前卵泡的侵入以及巨噬细胞、粒细胞和T淋巴细胞向黄体迁移的数据表明,调节性细胞因子的局部分泌可能参与调节黄体的形成、退化及其在妊娠早期的维持。多项证据表明,促炎细胞因子如白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)可调节黄体化过程中发生的类固醇生成变化。例如,在人或猪的颗粒细胞中,IL-1可抑制雌二醇(E2)的生物合成;在大鼠中,TNF-α可抑制;在牛中,IL-6可抑制。此外,IL-1可刺激孕酮(P4)的产生,但程度远低于促黄体生成素(LH),并且可刺激大鼠卵泡膜细胞合成前列腺素E2(PGE2)。IL-1和TNF-α能够降低牛黄体细胞的P4产生和存活率,这表明促炎细胞因子在控制黄体溶解机制中具有潜在相关性。与反刍动物不同,TNF-α对人黄体细胞没有影响,但可增强干扰素-γ(IFN-γ)诱导的P4分泌减少。最后,关于滋养层干扰素在反刍动物妊娠建立时维持黄体机制中的参与情况,目前已有相关数据。从这些观察结果和其他研究中,我们可以认为细胞因子参与了黄体功能的调节。

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