Protective Effects of Berberine on Bromobenzene-Induced Nephrotoxicity in Mice

Bromobenzene is an environmental toxin whose metabolites cause renal toxicity. The mechanism involved in toxicity includes oxidative stress. The aim of this study was to investigate the protective effects of berberine against bromobenzene-induced renal toxicity in male NMRI mice.

In this experimental study, subjects were divided into five groups. Group I: control: recipient of normal salineGroup II: recipient of bromobenzene at a dose of 0.36 ml/kg intraperitoneally on the tenth day. Third, fourth and fifth groups: recipient of berberine at doses of 25, 50, 100 mg/kg, orally for 10 days successively, and bromobenzene at a dose of 0.36 ml/kg intraperitoneally. 24 hours after the last administration, blood samples were taken from animals and renal markers were measured. The right kidney was used to measure markers of oxidative stress and the left kidney was used for histological studies.

The results of this study revealed that bromobenzene administration causes a significant increase in blood urea nitrogen creatinine, malondialdehyde and nitric oxide, as well as a significant reduction of glutathione levels and activity of catalase, superoxide dismutase and glutathione peroxidase enzymes than the control group (p<0.05). But berberine causes a significant decrease in blood urea nitrogen creatinine, malondialdehyde and nitric oxide, as well as a significant increase of glutathione levels and activity of catalase, superoxide dismutase and glutathione peroxidase enzymes than the bromobenzene group (p<0.05).

The present study indicates that treatment with berberine significantly improved renal function and reduced oxidative damage to kidney tissue in bromobenzene-induced toxicity.