Browsing by Author "Bora, Ejder Saylav"

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Caffeine Mitigates Tamoxifen-Induced Fatty Liver in Wistar Rats
(Acta Cirurgica Brasileira, 2024) Sezgin, Yasin; Bora, Ejder Saylav; Arda, Duygu Burcu; Uyanikgil, Yigit; Erbas, Oytun
Purpose: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats. Methods: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration. Results: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001). Conclusion: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.
Protective Effect of Dapagliflozin on Colistin-Induced Renal Toxicity
(Mre Press, 2021) Bora, Ejder Saylav; Erdogan, Mumin Alper; Meral, Ayfer; Karakaya, Zeynep; Erbas, Oytun
Objectives: Multiple-drug resistance to Gram-negative bacteria has increased significantly in recent years. Colistin is increasingly used as a last line of defense against these bacteria. However, colistin has been associated with nephrotoxicity in experimental animals. This study explores the protective effect of dapagliflozin in a rodent model of nephrotoxicity. Material Method: The present study includes a total of 24 male rats, of which 16 were given a single 20 mg/kg dose of colistin (Colimycin 150 mg/mL) intravenously to induce renal toxicity. The remaining eight rats were given no drugs in order to serve as the control, Group A. The 16 rats treated with colistin were then divided into two groups. Rats in Group B received 0.9% NaCl saline solution at a dose of 30 mL/kg/day intraperitoneally (i.p.) and 10 mg/kg/day dapagliflozin (Forziga 10 mg) via oral gavage. Those in Group C received 0.9% NaCl saline solution at an i.p. dose of 30 mL/kg/day. Both saline and dapagliflozin were administered as described over the course of ten days. The animals were euthanized and blood samples were taken by cardiac puncture for further analysis. Their kidneys were removed for histopathological and biochemical examination. Results: Levels of creatinine, BUN, KIM-1, and MDA were significantly increased in the 16-rat (Groups B and C) treatment group, in comparison to the control group; however, these biomarkers were significantly normalized in Group B, which had received dapagliflozin in addition to saline. The GSH levels of Group C showed significant decline when compared to those of the control group, and were significantly normalized in Group B. Histologically, in Group 2, we observed severe tubular dilatation and tubular epithelial cell injury in comparison to the control group. These severe anatomical changes were decreased in Group B. Conclusion: Apart from its positive effect on glucose regulation, which is the usual purpose of dapagliflozin, we observed that in colistin-induced nephrotoxicity, it decreases oxidative stress by inhibiting SGLT-2, and has restorative effects in terms of histopathology and biochemistry. These findings offer hope that the use of dapagliflozin may be protective for contrast nephropathy, which causes renal tubule damage through oxidative mechanisms. Future studies will further clarify the mechanistic action of colistin and dapagliflozin, and may support the hypothesis that dapagliflozin can be used as an adjunctive therapy in all nephrotoxic conditions.
Vincamine Mitigates Methotrexate-Induced Liver Fibrosis Model
(AVES, 2025) Urun, Yonca Yilmaz; Guner, Gurkan; Bora, Ejder Saylav; Taskin, Ayse Buket; Urun, Muslih; Erbas, Oytun
Background/Aims: Liver fibrosis is linked to higher rates of death and disease. This study examined the hepatoprotective properties of vincamine and its potential therapeutic application in treating liver damage caused by methotrexate in rats. Materials and Methods: Thirty male Wistar albino rats, with weights ranging from 150 to 200 g and ages between 10 and 12 weeks, were included in the study. A total of 10 rats were selected to serve as the control group, receiving no medication. A group of 20 rats was given a single intraperitoneal dose of 20 mg/kg methotrexate in order to cause liver damage. Subsequently, the participants were randomly allocated into 2 cohorts and administered either 1 mL/kg/day tap water or 50 mg/kg/day vincamine orally through gavage on a daily basis for a duration of 10 days. Following the completion of the treatment period, the animals were euthanized and their livers were examined histologically. Furthermore, the levels of plasma galectin-3 (gal-3), cytokeratin 18, malondialdehyde (MDA), alanine transaminase (ALT), liver MDA, and transforming growth factor beta (TGF-beta) levels were evaluated. Results: Treatment with vincamine resulted in a significant decrease in plasma gal-3, cytokeratin, MDA, and ALT levels and liver MDA and TGF-beta levels compared to the methotrexate and saline group. Vincamine treatment effectively protected against liver injury, and histopathological examination of the livers confirmed these results. Conclusion: This study demonstrates that vincamine alleviates methotrexate-induced liver toxicity via exhibiting antioxidant, antiinflammatory, and anti-fibrotic activities and improved liver functionally, biochemically, and histopathologically.