Karakus, SavasOzkaraca, Mustafa2024-10-262024-10-2620232636-7688https://doi.org/10.5455/annalsmedres.2023.09.264https://search.trdizin.gov.tr/tr/yayin/detay/1209351https://hdl.handle.net/20.500.12418/25070Aim: This study investigates the protective effects of Dinoprost against Ischemia/ Reperfusion (I/R) damage in the rat ovary, focusing on the expression of cyclooxygenase-2 (COX-2), Interleukin-1? (IL1?), and Tumor Necrosis Factor-? (TNF-?). Additionally, the impact of Dinoprost on reducing hemorrhage in the ovarian tissue is evaluated. Materials and Methods: A total of 24 rats were randomly divided into four groups: Control, Ischemia (Isch), I/R, and Dino+I/R. Ischemia was induced by clamping the ovarian blood supply, followed by reperfusion. Dinoprost was administered before reperfusion in the Dino+I/R group. COX-2, IL1?, and TNF-? expression levels were assessed through histochemical and immunochemical analyses. Hemorrhage in the ovarian tissue was also examined. Results: The Dino+I/R group exhibited a significant decrease in COX-2 expression compared to the Isch and I/R groups (p<0.05). However, there were no significant changes in the expression levels of IL1? and TNF-? among the groups. Notably, the Dino+I/R group showed significantly reduced hemorrhage compared to the Isch and I/R groups (p<0.05). Conclusion: Dinoprost demonstrated a protective effect against I/R damage in the rat ovary, primarily by attenuating COX-2 expression and reducing hemorrhage. These findings suggest the potential therapeutic utility of Dinoprost in mitigating ovarian I/R injury, emphasizing its role in preserving ovarian function and fertility.en10.5455/annalsmedres.2023.09.264info:eu-repo/semantics/openAccessDinoprostTissue damageIschemia/reperfusion injuryRat ovaryArticle30111458145251209351