Abstract

ObjectıvesThis study investigates whether Cloprostenol, a synthetic prostaglandin analog, could protect against ischemia/reperfusion (IR) injury in rat ovaries. MethodsAdult female rats were divided into four groups: Sham groups, ischemia (IS) groups, ischemia/reperfusion (IR) groups, and Cloprostenol-treated (CT) groups. The IR injury model was established by clamping the ovarian pedicle for a specified period, followed by reperfusion. The CT group received a pre-treatment of Cloprostenol before inducing ischemia. Ovarian tissues were collected for histological, and immunohistochemical examination. ResultsThe IS group exhibited severe morphological damage to ovarian tissues, including disrupted tissue architecture and increased apoptosis (p < 0.001). In contrast, the CT group displayed significantly improved ovarian histology, with notable preservation of ovarian tissue and reduced apoptotic activity (p < 0.01). Immunohistochemical analysis revealed that the levels of 8-Hydroxy-2-deoxyguanosine (8-OHdG), Caspase 3, Cyclooxygenase 2 (COX-2), and Interleukin 1 beta (IL-1β) staining, which were elevated in the IS and IR groups, were significantly diminished in the CT group (p < 0.05). ConclusıonCloprostenol administration before IR injury in rat ovaries demonstrated a remarkable protective effect by improving histological damage and reducing DNA damage inflammation. These results highlight the therapeutic potential of Cloprostenol in safeguarding ovarian health against IR.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.