Antioxidant and anti-inflammatory potential of vanillic acid improves nephrotoxicity induced by sodium arsenite in mice.

Abstract

This study examined the potential of vanillic acid (VA) to protect against renal oxidative stress and inflammation caused by sodium arsenite (SA) in mice. Mice were assigned to five groups: control, VA (100 mg/kg), SA (50 ppm in drinking water for 8 weeks), and SA + VA (50 and 100 mg/kg orally in the 7th and 8th weeks). After the experiment was ended, the Mice were sacrificed and serum and renal tissue samples were collected for additional assessments. Treatment with VA suppressed SA-induced increase in blood urea nitrogen and creatinine in the serum. Furthermore, renal histological damage induced by SA administration was ameliorated with VA treatment. Also, the increase in the level of lipid peroxidation marker (thiobarbituric acid reactive substances) along with the reduction in total thiol levels and the diminished activities of antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in the renal tissue of SA-treated mice were effectively reversed following treatment with VA. The results exhibited that the VA-treated groups (50 and 100 mg/kg) mitigated the elevation of inflammatory markers in kidney tissue (tumor necrosis factor-α and nitric oxide) in SA-exposed mice. Our research findings indicate that VA could be a potential therapeutic agent for the management of SA-associated nephrotoxicity.