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环氧化酶-2和半乳糖凝集素-3表达在绝经前子宫内膜息肉发病机制中的作用研究

Investigation of the Roles of Cyclooxygenase-2 and Galectin-3 Expression in the Pathogenesis of Premenopausal Endometrial Polyps.

作者信息

Kasap Esin, Karaarslan Serap, Gur Esra Bahar, Genc Mine, Sahin Nur, Güclü Serkan

机构信息

Department of Obstetrics and Gynecology, Sifa University School of Medicine, Izmir, Turkey.

Department of Patology, Sifa University School of Medicine, Izmir, Turkey.

出版信息

J Pathol Transl Med. 2016 May;50(3):225-30. doi: 10.4132/jptm.2016.03.08. Epub 2016 Apr 16.

Abstract

BACKGROUND

The pathogenesis and etiology of endometrial polyps has not been elucidated. In this study, we aimed to examine the pathogenic mechanisms of endometrial polyp development using immunohistochemistry. We evaluated the expression of galectin-3 and cyclooxgenase-2 (COX-2) during the menstrual cycle in premenopausal women with endometrial polyps or normal endometrium.

METHODS

Thirty-one patients with endometrial polyps and 50 healthy control patients were included in this study. The levels of expression of COX-2 and galectin-3 were studied by immunohistochemistry.

RESULTS

The percentage of COX-2-positive cells and the intensity of COX-2 staining in the endometrium did not vary during the menstrual cycle either in the control group or in patients with endometrial polyps. However, expression of galectin-3 was significantly lower in endometrial polyps and during the proliferative phase of the endometrium compared with the secretory phase.

CONCLUSIONS

Our data suggests that the pathogenesis of endometrial polyps does not involve expression of COX-2 or galectin-3.

摘要

背景

子宫内膜息肉的发病机制和病因尚未阐明。在本研究中,我们旨在通过免疫组织化学研究子宫内膜息肉发生的致病机制。我们评估了绝经前患有子宫内膜息肉或正常子宫内膜的女性在月经周期中半乳糖凝集素-3和环氧化酶-2(COX-2)的表达情况。

方法

本研究纳入了31例子宫内膜息肉患者和50例健康对照患者。通过免疫组织化学研究COX-2和半乳糖凝集素-3的表达水平。

结果

在对照组或子宫内膜息肉患者中,子宫内膜中COX-2阳性细胞的百分比和COX-2染色强度在月经周期中均无变化。然而,与分泌期相比,子宫内膜息肉中以及子宫内膜增殖期半乳糖凝集素-3的表达明显较低。

结论

我们的数据表明,子宫内膜息肉的发病机制与COX-2或半乳糖凝集素-3的表达无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de8/4876085/187987aa56f0/jptm-2016-03-08f1.jpg

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