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子宫内膜异位症与人类不孕:对在位内膜作用的新研究

Endometriosis and human infertility: a new investigation into the role of eutopic endometrium.

作者信息

Minici Francesca, Tiberi Federica, Tropea Anna, Orlando Mariateresa, Gangale Maria Francesca, Romani Federica, Campo Sebastiano, Bompiani Adriano, Lanzone Antonio, Apa Rosanna

机构信息

Cattedra di Fisiopatologia della Riproduzione Umana, Università Cattolica del Sacro Cuore (UCSC), 00168 Roma, Italy.

出版信息

Hum Reprod. 2008 Mar;23(3):530-7. doi: 10.1093/humrep/dem399. Epub 2007 Dec 19.

DOI:10.1093/humrep/dem399
PMID:18096563
Abstract

BACKGROUND

Endometriosis is related to infertility even in the absence of mechanical alterations of the reproductive tract. Even though the pathogenesis of this phenomenon is still unclear, an impaired endometrial receptivity has been recently suggested. The aim of the present study was to investigate if endometriotic peritoneal fluids (EPF) could interfere with endometrial stromal cell (ESC) decidualization and if tumor necrosis factor (TNF)-alpha could be involved in the EPF effect.

METHODS

Eutopic ESC were isolated from patients with or without endometriosis. ESC were treated with 17beta-estradiol 10(-8) M and 6alpha-methyl-17alpha-hydroxyprogesteroneacetate 2x10(-7) M for 16 days. In vitro decidualization was morphologically and biochemically assessed. We analysed whether ESC decidualization could be affected by EPF or peritoneal fluids from control patients (CPF), with or without soluble TNF-alpha receptor 1 (sTNFR-1).

RESULTS

Compared with ESC from control patients, eutopic ESC from patients with endometriosis showed an impaired decidualization. Decidualization of normal ESC was morphologically normal but biochemically abnormal in the presence of EPF, which was able to decrease the secretion of decidualization markers. sTNFR-1 was able to partially counteract this effect.

CONCLUSIONS

In endometriosis, the milieu surrounding the uterine cavity may be involved in impaired eutopic ESC decidualization, partially due to increased peritoneal levels of TNF-alpha.

摘要

背景

子宫内膜异位症即使在生殖道无机械性改变的情况下也与不孕相关。尽管这种现象的发病机制仍不清楚,但最近有人提出子宫内膜容受性受损。本研究的目的是调查子宫内膜异位症患者的腹腔液(EPF)是否会干扰子宫内膜基质细胞(ESC)的蜕膜化,以及肿瘤坏死因子(TNF)-α是否参与EPF的作用。

方法

从有或无子宫内膜异位症的患者中分离出在位ESC。将ESC用10⁻⁸ M的17β-雌二醇和2×10⁻⁷ M的6α-甲基-17α-羟基孕酮醋酸酯处理16天。对体外蜕膜化进行形态学和生化评估。我们分析了ESC的蜕膜化是否会受到EPF或对照患者的腹腔液(CPF)的影响,有无可溶性TNF-α受体1(sTNFR-1)。

结果

与对照患者的ESC相比,子宫内膜异位症患者的在位ESC显示出蜕膜化受损。在存在EPF的情况下,正常ESC的蜕膜化形态学正常但生化异常,EPF能够降低蜕膜化标志物的分泌。sTNFR-1能够部分抵消这种作用。

结论

在子宫内膜异位症中,子宫腔周围的环境可能参与在位ESC蜕膜化受损,部分原因是腹腔内TNF-α水平升高。

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