Investigation of Podocalyxin and Urotensin-2 levels in kidney tissues of rats treated with diclofenac sodium

The kidney is a partially cyclooxygenase (COX)-dependent organ. PGs play an active role in the regulation of vascular resistance in the kidney and in the provision of water-salt homeostasis by regulating glomerular hemodynamics and distal nephron functions. In our experimental study, we aimed to reveal the oxidative damage caused by diclofenac sodium, a non-selective nonsteroidal anti-inflammatory drug, in the kidney by biochemical and immunohistochemical methods. In the study, 14 female Wistar Albino rats, divided into 2 groups, 7 diclofenac sodium and 7 control, were used. Rats in the control group were injected with 1ml/kg 0.9% saline intraperitoneally (i.p) every day for 5 days. Rats in the diclofenac sodium group were administered 50mg/kg diclofenac sodium intramuscularly (i.m) every day for 5 days. After sacrificing, TAS and TOS were performed as biochemical analyses. TAS levels were statistically significantly decreased in the diclofenac sodium group compared to the control group (p<0.001). Serum TOS levels were statistically significantly increased in the diclofenac group compared to the control group (p<0.001). Histopathological and immunohistochemical examinations were also performed. Compared to the control group, marked atrophy in the glomeruli and a decrease in Bowman's space; degeneration in the proximal and distal tubule epithelium and hyaline cysts were observed in the diclofenac sodium group. After immunohistochemical staining, Podocalyxin (PODXL) and Urotensin II (U II) immunoreactivity and histoscoring were found to be statistically significantly increased in the study group (p<0.001). As a result, it was obtained that diclofenac sodium, when given at a dose of 50 mg/kg/day, developed acute renal failure in rats, caused histopathological changes, and also significantly increased PODXL and U II immunoreactivity in the study group.