Investigating the protective potential of dinoprost in a rat model of ischemia-reperfusion

Abstract

Aim: 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-1β (IL1β), and Tumor Necrosis Factor-α (TNF-α). 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, IL1β, and TNF-α 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 IL1β and TNF-α 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.