Objective To investigate the stimulation effect and mechanism of uric acid induce the response of inflammation in prostatic epithelial cells (RWPE-1 cells). Methods Prostatic epithelial cells (RWPE-1 cells) were cultured with uric acid at concentrations of 0, 8, 12 and 16 mg/dl. The proliferation and morphological changes of RWPE-1 cells were observed by an inverted microscope. Western blotting method was used to detect protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor-κB p65(NF-κBp65), inhibitor of nuclear factor-κB kinase subunit alpha (IKKα), inhibitor of nuclear factor-κB kinase subunit beta (IKKβ) and nucleotide oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) in RWPE-1 cells. Gene expression of IKKα, IKKβ, NLRP3 and Caspase-1 was quantified by real-time polymerase chain reaction. Cell culture supernatants were measured for inflammatory interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) by enzyme linked immunosorbent assay (ELISA). Results Morphological changes in RWPE-1 cells were concentration-dependent with uric acid from inverted microscopy. Compared with untreated RWPE-1 cells, the levels of TLR4, NF-κBp65, IKKα, IKKβ and NLRP3 in the uric acid-stimulated group were elevated, and the levels of TLR4, NF-κBp65, IKKα, IKKβ and NLRP3 were signaficantly correlated with uric acid concentration(P 0.05). After 24 h, the TNF-α levels of each group were (24.86±0.61), (25.14±0.83), (30.34±0.61), (30.77±1.84) ng/L, IL-1β were (14.81±0.23), (15.53±0.30), (22.87±0.65), (25.60±0.70) ng/L. After 48 h, the TNF-α of each group were (26.72±0.37), (26.80±1.14), (31.60±0.76), (42.98±1.49) ng/L, IL-1β were (25.36±0.70), (30.29±0.62), (38.91±1.52), (40.97±1.17) ng/L. After 24 and 48 hours of uric acid stimulation, high concentration of uric acid enhances the expression levels of IL-1β and TNF-α in RWPE-1 cells (P<0.05). Conclusion Uric acid can induce inflammatory response in RWPE-1 cells, and activation of TLR4/NF-κB and NLRP3/Caspase-1 signaling pathways is one of the mechanisms. Key words: Uric acid; RWPE-1 cell; Inflammatory response; Toll-like receptor 4/nuclear factor-κB signaling pathway; Nucleotide oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)/Caspase-1 signaling pathway