Abstract
BACKGROUND: Diquat (DQ) exposure can cause acute kidney failure and rhabdomyolysis. Accordingly, the current study aimed to assess how DQ toxicity affects the viability of human proximal tubular cells (HK-2) and to evaluate the potential protective effects of Tannic acid (TA) in this experimental model. METHODS: HK-2 cells were divided into groups: negative control, positive control, DQ alone, and DQ combined with TA at concentrations of 0.5, 2.5, and 5 μmol/L for 24 h. Subsequently, cell viability, reactive oxygen species (ROS) production, oxidative stress and inflammatory marker concentrations, as well as the expression of apoptosis-related genes, were evaluated in all groups. RESULTS: The data indicate that DQ significantly increased ROS production and elevated the levels of malondialdehyde (MDA) and interleukin-6 (IL-6), which were associated with increased expression of BCL2 associated X protein (BAX) and cleaved caspase-3 genes in HK-2 cells. Additionally, DQ exposure led to significant decreases in total antioxidant capacity (TAC), interleukin-10 (IL-10) levels, and B-cell lymphoma 2 (Bcl-2) anti-apoptotic gene expression. TA treatment inhibited oxidative stress, inflammation, and apoptosis, likely through the BAX/Bcl-2 and caspase-3/cleaved caspase-3 signaling pathways in renal cells. CONCLUSION: According to the results, TA treatment at all tested concentrations enhanced the expression of anti-apoptotic genes and suppressed cell apoptosis, thereby increasing renal cell viability.