ArticleBiomedical engineering online2025
Tannic acid inhibits diquat induced human renal HK-2 cells apoptosis through BAX/Bcl2/caspase/cleaved caspase-3 signaling pathway.
Article in Biomedical engineering online, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiquat (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.
methodsHK-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.
resultsThe 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.
conclusionAccording 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.
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