Berberine alleviates sodium arsenite-induced renal and liver toxicity by regulating oxidative stress and inflammation in rats

BackgroundArsenic is ubiquitous in the environment, and long- or short-term exposure through water, food, and occupational sources can contribute to oxidative stress-related injuries. We investigated berberine (BBR, as a natural anti-oxidant) protective effects against sodium arsenite (NaAsO2) related damage.MethodsAnimals were allocated to five groups. Group 1 was used as a control. Group 2 received NaAsO2 (10 mg/kg P.O., for 3 weeks). Groups 3, 4, and 5 received oral administration of BBR (25, 50, and 100 mg/kg, respectively) within 4 weeks + NaAsO2 (10 mg/kg P.O., for 3 weeks). Twenty-four h after the last administration, markers of renal and liver function, oxidative stress, and inflammatory factors were measured.ResultsNaAsO(2) exposure significantly increased hepatic enzymes, like ALT, ALP, and AST as well as markers of renal function, like creatinine and BUN, oxidative damage markers, like malondialdehyde, nitric oxide, and inflammatory markers, like NF-kB level, interleukin-1 beta, and tumor necrosis factor-alpha. Furthermore, NaAsO2 caused a significant reduction in anti-oxidant markers (glutathione content, glutathione peroxidase, catalase, and superoxide dismutase). The administration BBR + NaAsO2 caused a significant change in these factors compared to the arsenic group.ConclusionThe BBR treatment exerted a significant protective effect on NaAsO2-related hepatorenal toxicity. These protective effects of BBR are possible because of a reduction in inflammation and oxidative stress markers.