4.5 Article

Ellagic acid increases implantation rates with its antifibrotic effect in the rat model of intrauterine adhesion

Journal

PATHOLOGY RESEARCH AND PRACTICE
Volume 246, Issue -, Pages -

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.prp.2023.154499

Keywords

Asherman Syndrome; Ellagic acid; Fibrosis; Intrauterine adhesion

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The study aimed to investigate the effect of ellagic acid (EA) on fibrosis in intrauterine adhesion (IUA) model rats and to increase endometrial receptivity. The results showed a decrease in fibrotic structure, down-regulation of TGFβ1 activity, up-regulation of BMP7 activity, and an increase in LIF expression and implantation rates in the EA-treated group compared to the control group. Therefore, it can be concluded that EA treatment reduces fibrosis and increases implantation rates in IUA by promoting uterine tissue healing and enhancing endometrial receptivity.
Intrauterine adhesions (IUA) are defined as the adhesion of opposing endometrial tissue with dense fibrous adhesive bands within the uterine cavity. With the increase in cesarean sections and endometrial surgical pro-cedures, intrauterine adhesions have become a problem with increasing incidence and decreasing implantation. The purpose of the study was to investigate the effect of ellagic acid (EA), a phenolic compound, on fibrosis in IUA model rats. Another goal of the study was to increase endometrial receptivity with EA. The groups in the study were planned as control, DMSO, EA, IUA, IUA+DMSO, and IUA+EA, with 8 Sprague Dawley rats in each group. EA was administered at a dose of 100 mg/kg/day for 35 days. At the end of the experiment, the uterine tissues of the rats were removed. Histochemical staining was used to validate the IUA model and determine the degree of fibrosis. The levels of some fibrosis-related genes and proteins in the obtained uterine tissues were evaluated. In addition, implantation rates were determined. In our findings, it was observed that the fibrotic structure was decreased in the treated IUA+EA group compared to the IUA group, while fibrotic improvement was supported by down-regulation of TGF & beta;1 activity and up-regulation of BMP7 activity. The increase in the expression of the endometrial marker LIF with EA treatment was consistent with the increase in implantation rates with treatment. As a result of the study, it can be said that EA applied as a treatment against IUA causes healing in uterine tissue by reducing fibrosis and increases implantation rates by increasing endometrial receptivity.

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