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    Effects of potentilla fulgens as a prophylactic agent for ischemia/reperfusion injury in the rat ovary
    (Science Printers and Publishers Inc., 2015) Toğrul C.; Balsak D.; Ekinci C.; Seçkin K.D.; Ekinci A.; Tahaoğlu A.E.; Bademkiran H.
    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.
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    Simvastatin treatment prevents cell damage and regulates angiogenesis in a rat ovarian torsion and detorsion model an immunohistochemical study of caspase-3 and sFlt-1 expression
    (Science Printers and Publishers Inc., 2020) Toğrul C.; Deveci E.
    OBJECTIVE: Ovarian torsion is a condition that affects the development of ovaries and restricts blood flow. It occurs most frequently in women of reproductive age, and delay in torsion resolution may result in necrosis and ovarian loss. Ischemia-reperfusion of ovarian tissue is known to cause oxidative damage. We aimed to investigate caspase-3 expression as it is involved in apoptosis and inflammation, and sFlt-1 which is responsible for endothelial dysfunction produced by various tissues. STUDY DESIGN: Wistar female rats (n=32) were randomly divided into 4 groups: control, ischemia, ischemia-reperfusion, and ischemia-reperfusion+simvastatin. In the control group, the ovaries were surgically opened and closed, then blood and ovarian tissues of the animals were taken. In the ischemia and ischemia-reperfusion groups, the ovaries were surgically opened, and the left ovaries were sealed for ischemia. After 2 hours of ischemia, blood flow was re-allowed for 2.5 hours of reperfusion. In the ischemia-reperfusion group treated with simvastatin (10 mg/kg), rats were given simvastatin orally after reperfusion, and blood and tissue specimens were taken after 3 hours. Malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) activities were determined in the ovarian tissue homogenates for each rat. RESULTS: In the simvastatin-administered group, MDA and GSH values decreased as compared to in the ischemia and ischemia-reperfusion groups. In the simvastatin-treated group, GSH values were increased. In the ischemia group, degenerated granular cells in the antral follicle, luteal cells in the corpus luteum, and intense inflammatory cells in the stromal region were positive for expression of caspase-3. In the ischemia-reperfusion group, caspase-3 expression was positive in oocyte, granular, and stromal cells. In the ischemia-reperfusion+simvastatin-treated group, caspase-3 expression was negative in the granular cells of the antral follicle. It was positive in some stromal cells and corpus luteum cells. In the ischemia-reperfusion group, there was an increase in the expression of sFlt-1 in the luteal cells of the corpus luteum and in the vascular endothelial and inflammatory cells. In the ischemia-reperfusion+simvastatin-treated group, follicle cells and cells in the corpus luteum showed decreased sFlt-1 expression, whereas sFlt-1 expression was positive in vascular endothelial cells. CONCLUSION: We suggest that simvastatin administration could prevent cell damage by affecting proapoptosis activation. Simvastatin administration may induce the regulation of angiogenesis. © Science Printers and Publishers, Inc.