Effects of potentilla fulgens as a prophylactic agent for ischemia/reperfusion injury in the rat ovary
Seçkin, Kerem Doğa
Tahaoğlu, Ali Emre
Bademkıran, Muhammed Hanifi
Yaman Görük, Neval
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CitationToğrul, C., Balsak, D., Ekinci, C., Seçkin, K. D., Ekinci, A., Tahaoğlu, A. E., ... & Deveci, E. (2015). Effects of Potentilla fulgens as a Prophylactic Agent for Ischemia/Reperfusion Injury in the Rat Ovary. Analytical and quantitative cytopathology and histopathology, 37(5), 310-316.
OBJECTIVE: To investigate the effects of Potentilla fulgens as a prophylactic agent on ischemia/reperfusion (I/R) injury in the rat ovary. STUDY DESIGN: A total of 32 Wistar rats were divided into 4 equal groups: (I) sham, (II) ischemia, (III) ischemia+reperfusion, and (IV) I/R+Potentilla fulgens. In groups I and II, ovary torsion was not performed and no drug was administered. In group III, 1 hour of ischemia and 2 hours of reperfusion were performed and no drug was given. Group IV received 400 mg/kg/day Potentilla fulgens intraperitoneally 5 days before I/R injury. RESULTS: The detorsion group showed preantral ovarian follicles and corpus luteum around the blood vessels and positive expression of vascular endothelial growth factor (VEGF). In the Potentilla fulgens group (IV) the stromal vascular endothelium with weak expression of VEGF was detected in small areas, and the ovarian follicles and the corpus luteum showed negative expression of VEGF. In the detorsion group the theca cells and apoptotic cells in preantral follicles showed positive expression of E-cadherin in the ovarian surface epithelium. Moreover, the E-cadherin expression was found to be positive in terms of follicular development, theca cells, granulosa cells, and corpus luteum. Potentilla fulgens, given after ischemic injury and apoptosis, was seen to decrease the effect of Bcl-2 expression. CONCLUSION: These results provide compelling evidence that the expression of E-cadherin in the ovary is an important component of ovarian function. © Science Printers and Publishers, Inc.