<![CDATA[Introduction: This research aims to determine whether genistein functions as an antiangiogenic and inflammatory modulator by decreasing levels of VEGFR2, TGF-β1, and COX-2 in the peritoneal fluid of mice with an endometriosis model. Methods: The study involved 32 healthy female Mus musculus mice, 20-30 g in weight and 2-3 months old, divided into eight groups: negative control group (healthy mice without treatment), an endometriosis model group (endometriosis-induced mice without genistein), and six treatment groups that received varying doses of genistein (0.13, 0.26, 0.52, 0.78, 1.04, and 1.3 mg/day, n=4). Measurement of VEGFR-2, TGF-β1, and COX-2 levels in endometriosis lesions in mouse models using an Enzyme Immunoassay (EIA), Mice enzyme-linked immunoassay (ELISA) Kit. Results: This study showed that the endometriosis model exhibited increased levels of VEGFR-2, TGF-β1, and COX-2. Administration of genistein significantly normalized these elevated levels. Genistein markedly reduced VEGFR-2, TGF-β1, and COX-2 levels in all the treatment groups. Conclusion: Genistein decreases levels of VEGFR-2, TGF-β1, and COX-2 in the peritoneal fluid of a mouse model of endometriosis by acting as an antiangiogenic and inflammatory modulator. Consequently, genistein holds potential as a therapeutic agent in the treatment of endometriosis.]]>
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