Protective Effect of Allopurinol on Experimental Ovarian Ischemia-Reperfusion Injury Model of Rats
Citation
Yurtçu, E., Togrul, C., & Deveci, E. (2020). Protective Effect of Allopurinol on Experimental Ovarian Ischemia-Reperfusion Injury Model of Rats. ANALYTICAL AND QUANTITATIVE CYTOPATHOLOGY AND HISTOPATHOLOGY, 42(1), 8-16.Abstract
OBJECTIVE: To investigate the effect of allopurinol on an experimentally induced ovarian ischemia-repel fusion model. STUDY DESIGN: Female rats in the estrous cycle (n= 32) were divided into sham, ischemia, ischemia-reperfusion, and ischemia-reperfusion + allopurinol-treated groups. In the sham group the ovaries were opened and closed. In the ischemia group the ovaries were sealed for 2-hour ischemia. In the ischemia-reperfusion group, after ischemia, 2.5 hours of reperfusion was done. In the ischemia-reperfusion + allopurinol group, 3 hours after ischemia-reperfusion, 50 mg/kg allopurinol was administered. RESULTS: In the allopurinol-administered group, MDA levels were decreased. GSH values were decreased in the ischemia and ischemia-reperfusion group but increased in the allopurinol-treated group as compared to the control group. Caspase-3 expression was positive in enlarged corpus luteum cells. sFlt-1 expression was positive in vascular endothelial cells between preantral and antral follicles and some macrophages but negative in granular cells. In the ischemia group, sFlt-1 expression was positive in degenerative preantral and antral follicle cells, endothelial cells, and intense inflammatory cells. In the ischemia-reperfusion group, increased sFlt-1 expression was observed in luteal cells of the corpus luteum, vascular endothelial, and inflammatory cells. In the ischemia-reperfusion +allopurinol group, granular cells and corpus luteum cells showed decreased sFlt-1 expression, while being positive in vascular endothelial cells. CONCLUSION: Allopurinol inhibits development of apoptosis and reduces oxidative load in the ischemia-reperfusion stage, thus protecting the ovary from damage.
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