dc.contributor.author | Yurtçu, Engin | |
dc.contributor.author | Toğrul, Cihan | |
dc.contributor.author | Deveci, Engin | |
dc.date.accessioned | 2021-11-01T15:05:06Z | |
dc.date.available | 2021-11-01T15:05:06Z | |
dc.date.issued | 2020 | |
dc.identifier.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. | en_US |
dc.identifier.issn | 0884-6812 | |
dc.identifier.uri | https://hdl.handle.net/11491/7109 | |
dc.description.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. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Sci Printers & Publ Inc | en_US |
dc.relation.ispartof | Analytical And Quantitative Cytopathology And Histopathology | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Allopurinol | en_US |
dc.subject | Caspase-3 | en_US |
dc.subject | FLT1 Protein | en_US |
dc.subject | Fms-like Tyrosine Kinase-1 | en_US |
dc.subject | Ischemia | en_US |
dc.subject | Ischemia-reperfusion Injury | en_US |
dc.subject | Ovarian Diseases | en_US |
dc.subject | Ovarian Ischemia | en_US |
dc.subject | Ovarian Torsion | en_US |
dc.subject | Ovary | en_US |
dc.subject | Oxidative Stress | en_US |
dc.subject | Rats | en_US |
dc.subject | Reperfusion Injury | en_US |
dc.subject | sFlt-1 | en_US |
dc.subject | Vascular Endothelial Growth Factor Receptor-1 | en_US |
dc.title | Protective Effect of Allopurinol on Experimental Ovarian Ischemia-Reperfusion Injury Model of Rats | en_US |
dc.type | article | en_US |
dc.department | Hitit Üniversitesi, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümü | en_US |
dc.identifier.volume | 42 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.startpage | 8 | en_US |
dc.identifier.endpage | 16 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.department-temp | [Yurtcu, Engin] Karabuk Univ, Dept Obstet & Gynecol, Med Sch, Karabuk, Turkey; [Togrul, Cihan] Hitit Univ, Dept Obstet & Gynecol, Med Sch, Corum, Turkey; [Deveci, Engin] Dicle Univ, Dept Histol & Embryol, Med Sch, Univ St, Diyarbakir 21280, Turkey | en_US |
dc.contributor.institutionauthor | Toğrul, Cihan | |
dc.description.wospublicationid | WOS:000531823600002 | en_US |
dc.description.scopuspublicationid | 2-s2.0-85089374672 | en_US |