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

• DOI: 10.3892/mmr.2021.12368
• Publication Date: 2021-08-13T07:54:50Z
• Authors: Dongdong Li; Luobing Wang; Jiaoying Ou; Chuanxu Wang; Jiabao Zhou; Lili Lu; Yanshneg Wu; Jiandong Gao
• Keywords: 0303 health sciences; Caspase 3; bcl-X Protein; Apoptosis; Epithelial Cells; Articles; Rats; Uric Acid; 03 medical and health sciences; NLR Family, Pyrin Domain-Containing 3 Protein; Animals; NIMA-Related Kinases; Reactive Oxygen Species; Signal Transduction

Increasing uric acid (UA) could induce renal tubular epithelial cell (NRK‑52E) injury. However, the specific mechanism by which UA induces injury remains unknown. It was hypothesized that through reactive oxygen species (ROS) and Never in mitosis gene A (NIMA)‑related kinase 7 (NEK7)/NLR family pyrin domain containing 3 (NLRP3) signaling pathway. TUNEL assay flow cytometry were applied to measure apoptosis, results of present study showed treatment induced apoptosis NRK‑52E cells a concentration‑dependent manner. Western blotting performed determine expression levels cleaved caspase‑3, Bax Bcl‑xl, it found significantly increased after cells. ROS predominantly there an association between apoptosis. Enhanced NEK7, NLRP3, apoptosis‑associated speck‑like caspase‑1 observed treated with UA. The inhibitor, N‑acetyl‑l‑cysteine, exerted protective effect on UA‑induced reducing excess production, inhibited NEK7 NLRP3 inflammasome activation. These indicated activates might be related regulation NEK7/NLRP3