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与接受体外受精治疗的患者相比,正常排卵女性卵泡内基质金属蛋白酶及其抑制剂的表达情况。

Intrafollicular expression of matrix metalloproteinases and their inhibitors in normally ovulating women compared with patients undergoing in vitro fertilization treatment.

作者信息

D'Ascenzo Sandra, Giusti Ilaria, Millimaggi Danilo, Marci Roberto, Tatone Carla, Cardigno Colonna Rosella, Moscarini Massimo, Pavan Antonio, Dolo Vincenza, Caserta Donatella

机构信息

Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy.

出版信息

Eur J Endocrinol. 2004 Jul;151(1):87-91. doi: 10.1530/eje.0.1510087.

Abstract

OBJECTIVE

To assess possible differences in the activity of matrix metalloproteinases (MMPs), MMP-2 and MMP-9, and their inhibitors, the tissue inhibitors of MMPs, TIMP-1 and TIMP-2, in follicular fluid (FF) of women undergoing in vitro fertilization (IVF) treatment and of normally ovulating women.

DESIGN

Prospective study.

METHODS

MMP-2 and MMP-9 activity was analyzed by gelatin zymography and MMP-2, MMP-9, TIMP-2, TIMP-1 and 17beta-estradiol levels were measured in FF by ELISA.

RESULTS

We found significantly reduced MMP levels in FF of women undergoing IVF treatment when compared with those of normally ovulating women. In contrast, the TIMP-1 levels were found significantly increased in FF from IVF patients vs normally ovulating women. No significant differences were found for TIMP-2 between the two groups.

CONCLUSIONS

These findings underline a marked difference in MMPs and their inhibitors in the IVF women and the control group. Therefore we assume MMPs depend on hormonal steroidogenesis modulation induced by the gonadotropin protocol for IVF treatment.

摘要

目的

评估接受体外受精(IVF)治疗的女性与正常排卵女性卵泡液(FF)中基质金属蛋白酶(MMPs)、MMP - 2和MMP - 9及其抑制剂基质金属蛋白酶组织抑制剂(TIMPs)、TIMP - 1和TIMP - 2活性的可能差异。

设计

前瞻性研究。

方法

通过明胶酶谱法分析MMP - 2和MMP - 9活性,并采用酶联免疫吸附测定法(ELISA)检测卵泡液中MMP - 2、MMP - 9、TIMP - 2、TIMP - 1和17β - 雌二醇水平。

结果

我们发现,与正常排卵女性相比,接受IVF治疗的女性卵泡液中MMP水平显著降低。相比之下,IVF患者卵泡液中的TIMP - 1水平较正常排卵女性显著升高。两组之间TIMP - 2未发现显著差异。

结论

这些发现突显了IVF女性与对照组在MMPs及其抑制剂方面的显著差异。因此,我们推测MMPs依赖于IVF治疗中促性腺激素方案诱导的激素甾体生成调节。

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