Author/Authors :
-، - نويسنده Gaziosmanpasa University Faculty of Medicine, Department of Physiology, Tokat Turkey Erbas, Oytun , -، - نويسنده Izmir Dr Behcet Uz Pediatric Medicine and Surgery Training and Research Hospital, Pediatric Endocrinology Clinic, Izmir, Turkey Korkmaz, Huseyin Anil , -، - نويسنده Ege University School of Medicine, Department of Histology and Embryology, Izmir, Turkey Oltulu, Fatih , -، - نويسنده Ege University School of Medicine, Department of Histology and Embryology, Izmir, Turkey Aktug, Hüseyin , -، - نويسنده Ege University School of Medicine, Department of Histology and Embryology, Izmir, Turkey Yavasoglu, Altug , -، - نويسنده Ege University School of Medicine, Department of Gynecology and Obstetrics, Izmir, Turkey Akman, Levent , -، - نويسنده Gaziosmanpasa University Faculty of Medicine, Department of Neurology, Tokat, Turkey Solmaz, Volkan , -، - نويسنده Ege University Faculty of Medicine, Department of Physiology, Izmir, Turkey Taskiran, Dilek
Abstract :
Objective(s):The purpose of the present study was to investigate the protective effect of oxytocin on cisplatin (CP)-induced renal damage in rats. Materials and Methods: Fourteen adult Sprague Dawley rats, weighing 200 to 210, were administered by cisplatin (CP, 2 mg/kg/day) twice a week for five weeks. Then, they were randomly divided into two groups and treated with either saline (1 ml/kg/day) or OT (200 µg/kg/day) for five weeks. Seven rats served as control group. At the end of the treatment period, animals were sacrificed and their kidneys were assessed histologically. In addition, C-reactive protein (CRP), TGF-β and Akt expression were evaluated immunohistochemically. Results:Both tubules and glomeruli were found to be severely damaged with marked medullary tubulo-interstitial inflammation due to chronic cisplatin exposure, particularly in the saline-treated group (Group 1) compared to control group. Oxytocin treatment spared renal tissue significantly by suppressing CRP and TGF-β, and enhancing Akt expression. Conclusion: We conclude that renal damage due to cisplatin toxicity was prevented to a great extent by the anti-inflammatory effect of oxytocin.
