Background and objective: Acute pyelonephritis (APN) accounts for about 50%-60% of all pyelonephritis. In this study, the APN model of E. coli infection was established to analyze the significance of NLRP3 and lay a foundation for the clinical study of NLRP3 in the future. Materials and methods: 30 SD rats were assigned into model group (MG), control group (CG) and research group (RG). CG was fed normally without treatment. MG and RG were modeled with APN, and RG was additionally injected with MCC950 through the tail vein. Body temperature, weight, and NLRP3 mRNA, IL-1 beta and IL-18 levels were measured after modeling. White blood cells (WBC), lymphocytes (LYM), macrophages( M), neutrophils (NE) and eosinophils (E) in bladder lavage fluid, and NLRP3 protein expression in renal tissue were also detected. Results: The physical signs of CG did not change evidently during the experiment (P>0.05). The body temperature increased and the weight decreased in MG, while the reverse was observed in RG. T3 witnessed no evident differences in NLRP3 mRNA, IL-1 beta and IL-18 between RG and CG, which were lower versus MG. The weight of kidney was the highest in MG. however, the colony count of bladder fluid and kidney tissue in MG was evidently higher versus RG. NLRP3 protein expression in kidney tissue in RG was higher than CG and lower than MG. Conclusions: NLRP-3 is essential in E. coli-induced APN. Inhibition of NLRP-3 can effectively alleviate the inflammatory process of APN and repair damaged kidney tissue.