Research Information System
Tropical Journal of Pharmaceutical Research, vol.23, no.7, pp.1077-1082, 2024 (SCI-Expanded, Scopus)
Purpose: To investigate the potential protective effect of roxadustat against cisplatin-induced acute kidney injury (AKI) by evaluating biochemical markers, inflammatory parameters, renal function tests, and histopathological changes. Methods: Thirty female Wistar rats were randomized into control group, cisplatin with tap water group, and cisplatin with roxadustat group. Cisplatin-induced AKI was established by intraperitoneal injection of cisplatin at 10 mg/kg for seven days. Roxadustat was administered orally at 20 mg/kg/day to the treatment group. Blood and kidney samples were collected for biochemical and histopathological analyses respectively. Results: Roxadustat treatment significantly reduced markers of renal injury (malondialdehyde (MDA), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), transforming growth factor-beta 1 (TGF-beta1)), inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-18 (IL-18)) compared to the cisplatin group (p < 0.005). In addition, roxadustat treatment also improved renal function (blood urea nitrogen (BUN), serum creatinine (SCr)) compared to the cisplatin group (p < 0.005). Histopathological examination revealed a significant decrease in tubular epithelial necrosis and luminal necrotic debris in the roxadustat-treated group (p < 0.005). However, there was no significant difference in tubular dilatation and interstitial inflammation between groups (p > 0.05). Conclusion: Roxadustat significantly prevents cisplatin-induced AKI by attenuating renal injury, reducing inflammation, and improving renal function. This evidence suggests that roxadustat may be a promising preventive option for patients receiving cisplatin chemotherapy.