RESUMO
Increasing uric acid (UA) could induce renal tubular epithelial cell (NRK52E) injury. However, the specific mechanism by which UA induces renal tubular epithelial cell injury remains unknown. It was hypothesized that UA induces renal tubular epithelial cell injury through reactive oxygen species (ROS) and the Never in mitosis gene A (NIMA)related kinase 7 (NEK7)/NLR family pyrin domain containing 3 (NLRP3) signaling pathway. TUNEL assay and flow cytometry were applied to measure apoptosis, and the results of the present study showed that UA treatment induced apoptosis of NRK52E cells in a concentrationdependent manner. Western blotting was performed to determine the expression levels of cleaved caspase3, Bax and Bclxl, it was found that levels were significantly increased after UA treatment in NRK52E cells. ROS and apoptosis were predominantly induced in NRK52E cells and there was an association between ROS and apoptosis. Enhanced expression of NEK7, NLRP3, apoptosisassociated specklike and caspase1 were observed in NRK52E cells treated with UA. The ROS inhibitor, Nacetyllcysteine, exerted a protective effect on the UAinduced apoptosis of tubular epithelial cells by reducing excess ROS production, which significantly inhibited NEK7 and NLRP3 inflammasome activation. These results indicated that UA activates ROS and induces apoptosis of NRK52E cells. The mechanism might be related to the regulation of the NEK7/NLRP3 signaling pathway.