@article{article_1730683, title={Ovarian Ischemia-Reperfusion Injury and the Potential Role of Mangiferin: A Histopathological, Biochemical Investigation}, journal={Kocaeli Üniversitesi Sağlık Bilimleri Dergisi}, volume={11}, pages={160–166}, year={2025}, DOI={10.30934/kusbed.1730683}, author={Ayaz, Hayat and Aşır, Fırat}, keywords={Anti Müllerian Hormon, Histopatoloji, İskemi Reperfüzyon Hasarı, Mangiferin, Over}, abstract={Objective: Ischemia-reperfusion (IR) injury in the ovary can cause significant structural damage and compromise ovarian reserve by disrupting follicular integrity. This study aimed to investigate the protective effects of Mangiferin, a natural antioxidant and anti-inflammatory compound, in a rat model of ovarian IR injury. Histopathological evaluation, follicle counts, and serum anti-Müllerian hormone (AMH) levels were used to assess treatment efficacy.
Methods: Thirty-two female Sprague-Dawley rats were divided into Control, Mangiferin, IR, and IR+ Mangiferin. Ovarian IR was induced by bilateral clamping of the ovarian vasculature for 3 hours, followed by 3 hours of reperfusion. Mangiferin (20 mg/kg) was administered intraperitoneally once daily for 15 days. Ovarian tissues were subjected to histological analysis with follicle counts and AMH levels were measured using ELISA.
Results: The IR group exhibited marked histopathological changes, including vascular congestion, hemorrhage, edema, inflammatory cell infiltration, and extensive follicular degeneration. In contrast, the IR+ Mangiferin group showed improved tissue architecture, higher follicle counts, and AMH levels that were significantly preserved compared to the IR group. Conclusion: Mangiferin may reduce ovarian damage caused by IR injury and contribute to the preservation of ovarian reserve. These findings suggest a potential therapeutic benefit of Mangiferin in protecting ovarian tissue under ischemic conditions.}, number={3}, publisher={Kocaeli Üniversitesi}, organization={Dicle University Scientific Research Platform (DUBAP) (BAP Project no: TIP.24.028)}