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

Author:

Saribas Gulistan Sanem1ORCID,Dizakar Ozen Akarca2,Ozogul Candan3,Celik Ekin4,Ergoren Mahmut Cerkez5

Affiliation:

1. Ahi Evran Universitesi Tip Fakultesi

2. Bakircay Universitesi

3. University of Kyrenia: Girne Universitesi

4. Kirsehir Ahi Evran Universitesi

5. Near East University: Yakin Dogu Universitesi

Abstract

Abstract Background: 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 procedures, 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. Methods and Results: 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. 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 TGFβ1 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. Conclusions: 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.

Publisher

Research Square Platform LLC

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