Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway.

ABSTRACT: Increasing uric acid (UA) could induce renal tubular epithelial cell (NRK‑52E) 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 NRK‑52E cells in a concentration‑dependent manner. Western blotting was performed to determine the expression levels of cleaved caspase‑3, Bax and Bcl‑xl, it was found that levels were significantly increased after UA tr

SUBMITTER: Li D 

PROVIDER: S-EPMC8383041 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature