Nephroprotective effects of chlorogenic acid against sodium arsenite-induced oxidative stress, inflammation, and apoptosis

Background: Chronic exposure to arsenic (As) leads to serious renal disorders. Chlorogenic acid (CGA), a phenolic compound, has several well known physiological benefits, including antioxidant and anti-inflammatory activities. The present study investigated the potential renoprotective effects of CGA on sodium arsenite (NaAsO₂ )-induced kidney damage in mice. The mice were randomly allocated into five groups to receive daily treatment with CGA (200 mg kg^-1 ), NaAsO₂ (5 mg kg^-1 ), NaAsO₂ + CGA (100 mg kg^-1 ), NaAsO₂ + CGA (200 mg kg^-1 ), or a control for 28 days.

Results: In the NaAsO₂ -treated group, NaAsO₂ induced significant renal dysfunction, oxidative damage, inflammation, and apoptosis, as demonstrated by marked increases in urea and creatinine levels accompanied by a decrease in the kidney index. Considerable increases in malondialdehyde and nitric oxide levels and parallel decreases in various antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) levels were also detected in the renal tissues of NaAsO₂ -treated mice. NaAsO₂ exposure was associated with marked increases in renal inflammatory markers (interleukin-1β and tumor necrosis factor-α) and apoptosis indicators including Bax and caspase-3 levels contaminant, with a marked decrease in Bcl-2, an anti-apoptotic protein, in the NaAsO₂ -treated group compared with the control group. However, pretreatment with CGA substantially mitigated the renal injury and dysfunction associated with NaAsO₂ exposure by reducing tissue inflammation and apoptosis and improving the antioxidant status. The CGA pretreatment also alleviated the NaAsO₂ -induced histological alterations in renal tissues.

Conclusion: Taken together, our results suggest the efficacy of CGA in alleviating As-mediated renal tissue damage. © 2020 Society of Chemical Industry.

Keywords: apoptosis; arsenite; chlorogenic acid; nephrotoxicity; oxidative stress.