Harmaline improved oxidative stress and inflammation markers in nephrotoxicity induced by bisphenol-A in human renal tubular epithelial cells

Objectives: Bisphenol A (BPA) is a toxic agent which affects the kidney nephrons through inflammation and apoptosis in kidney cells. Harmaline has remarkable anti-inflammatory and anti-oxidative stress properties. Accordingly, the aim of the present study was to investigate the antioxidant effect of harmaline against nephrotoxicity caused by BPA in human kidney 2 (HK-2) cells. Materials and Methods: HK-2-cells were considered in the following groups: Control, bisphenol and harmaline with concentrations of 50, 100 and 200 mM. The cytotoxicity was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis method. Reactive oxygen species generation was measured by the flow cytometry technique. Total antioxidant capacity (TAC) and malondialdehyde (MDA) levels were measured using a spectrophotometric method. Anti-inflammatory and pro-inflammatory cytokines were measured using the enzyme-linked immunosorbent assay method. Results: The present study showed that exposure of HK-2 cells to BPA causes nephrotoxicity by reducing cell viability and increases in free radicals, which were associated with an increase in the MDA level and a decrease in the TAC concentration compared to the control group. In harmaline co-treatment groups, production of free radicals and MDA levels significantly decreased, and TAC levels significantly increased compared to the bisphenol A (BSA) group. Interleukin (IL)-6 level showed a remarkable increase in cells exposed to BPA. Although the IL-10 concentration significantly decreased compared to the control. Harmaline in all concentrations significantly decreased the IL-6 and increased IL-10 compared to the BPA cells. Conclusion: The results of this study confirmed the protective effects of harmaline in preventing inflammation, oxidative damage and toxicity caused by BPA in renal epithelial cells.