Ovarian torsion is an important reproductive gynecological emergency in daily life and physiology. Granulocyte colony stimulating factor (G-CSF) is a glycoprotein capable of hematopoietic development and successfully used in the treatment of congenital granulocytopenia. In our study, we aimed to investigate protective effects of G-CSF on ovarian ischemia reperfusion (IR) immunohistochemically. Four groups were used. In control group, abdomen was opened and closed with the surgical protocol. The rats in the G-CSF group were given 100 µg/kg G-CSF subcutaneously before the IR and the abdomen was surgically opened and closed. 3-h of ischemia was and then 3-h reperfusion was induced in the ischemia-reperfusion (I/R) group. In the IR+G-CSF group, 100 µg/kg G-CSF was given before the procedure and IR was performed. At the end of the experiment, ovarian tissues were fixed in 10% formalin and then processed for routine paraffin tissue protocol. Normal ovarian histology was observed in the control and G-CSF groups. In the IR group, vascular dilatations, hemorrhage and increased inflammation were observed. In the I/R+G-CSF group, pathology in seen IR was decreased. IL-6 expression was mainly negative in control and G-CSF groups. Positive IL-6 immune reaction was observed in the granulosa cells and stromal area. In the I/R+G-CSF group, IL-6 expression was significantly decreased in ovarian follicular structures and in the stromal area compared to the I/R group. In conclusion, G-CSF reduced vascular dilatation and inflammation in the ovarian IR model and promoted ovarian folliculogenesis. Keywords: Ovary, Ischemia/reperfusion, G-CSF, Azan, IL-6, Immunohistochemistry

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Aim: To examine the effects of gallic acid (GA) in the stomach in rats undergoing intestinal ischemia/reperfusion (IR) with Beclin -1 immunostaining. Material-Metod: 24 male Wistar albino rats were divided into control, IR and IR+GA groups. For the IR protocol, 60 minutes of ischemia and reperfusion were applied. The small intestines of the rats in the control group were removed by laparotomy and the abdomen was closed without applying anything else. Ischemia and reperfusion was applied to the superior mesenteric artery (SMA) for 60 minutes with a clamp in rats in the IR group. The blood flow was stopped with a clamp on the SMA of the rats in the IR+GA group and ischemia was applied for 60 minutes. 50 mg/kg gallic acid was given intraperitoneally to the animals, 60 minutes of reperfusion was performed, and the abdomen was closed. The stomach tissues were placed in paraffin blocks after routine histological follow-ups. Five micrometer-thick sections were taken from the paraffin blocks and stained with Hematoxylin-eosin and Beclin-1 immunostaining. Results: In the IR group, degeneration of gastric folds, apoptosis of epithelial cells and degeneration of lamina muscularis were observed. In the IR + GA group, gastric folds improved, but cell infiltration in the lamina propria and degeneration in the muscular layer were observed. Beclin-1 expression was positively observed in the surface epithelial cells and gastric glands in the control group. In the IR group, it was observed that the gastric folds were positive on the surface cells and negative in the submucosa, while in the IR + GA group, it was intensely expressed in the gastric epithelium and gastric glands. Conclusion: By increasing the expression of beclin-1, GA treatment induced autophagy in gastric mucosal cells, triggered the destruction of damaged cells and provided restoration of the mucosal layer. Keywords:   Beclin-1, gallic acid, apoptosis