Hesperidin protects against diethylnitrosamine-induced nephrotoxicity through modulation of oxidative stress and inflammation

Abstract

Background: Kidney forms the main controlling organ in sustaining homeostasis and, thus, is vulnerable to toxicity by xenobiotics. Aims and Objective: To evaluate the possible protective effects of the citrus flavonoid, hesperidin (HES), against diethylnitrosamine (DEN)-induced nephrotoxicity in rats. Materials and Methods: Rats received a single intraperitoneal dose of DEN (200 mg/kg body weight). Two-weeks after DEN administration, rats received 0.5 g/L phenobarbital in drinking water for 12 weeks. HES (50, 100, and 200 mg/kg body weight) were orally administered from the first day of experiment. Result: DEN administration induced nephrotoxicity evidenced or DEN-induced nephrotoxicity was evidenced by the histological alterations and significant increase in serum creatinine (P o 0.001), urea (P o 0.01), and uric acid (P o 0.001) levels. DEN-intoxicated rats exhibited a significant (P o 0.001) increase in renal lipid peroxidation levels and reduced glutathione content and activity of superoxide dismutase, glutathione peroxidase, and glutathione-Stransferase. Concomitant supplementation with all the doses of HES markedly prevented DEN-induced biochemical and histopathological alterations. Conclusion: The study findings provide evidence that HES could protect against DEN-induced renal injury through abolishment of inflammation and oxidative stress and potentiation of the antioxidant defense system.