〔Abstract〕 Objective To explore the effect and mechanism of palmitic acid sodium(PA) exposure for different time on HK-2 cells injury. Methods CCK-8 assay was used to detect the activity of HK-2 cells treated with PA at different times; oil red staining was used to detect lipid deposition at different time of PA treatment; Annexin-Ⅴ-FITC/PI apoptosis kit was used to detect the apoptosis of HK-2 cells treated with PA at different times; reactive oxygen species(ROS) production was detected by ROS kit at different time of PA treatment; ELISA was used to detect GSH and SOD in cells as well as the levels of IL-1β and IL-18 in the cell supernatant; Western blot was used to determine the expressions of NLRP3, ASC, Caspase-1 and NOX4 in HK-2 cells. Results CCK-8 assay showed that HK-2 cell viability decreased in PA(6, 9, 12, 24 h) groups; oil red staining showed that lipid deposition increased in PA(6, 9, 12, 24 h) groups; Annexin-Ⅴ-FITC/PI apoptosis kit results showed that the apoptosis rate increased; ROS kit results showed that ROS production significantly increased in PA(6, 9, 12, 24 h) groups; ELISA results showed that the activities of GSH and SOD decreased in PA(6, 9, 12, 24 h) groups, while the levels of IL-1β and IL-18 in supernatant increased; Western blot results showed that the expression levels of inflammatory related proteins NLRP3, Caspase-1, ASC and NOX4 in PA(6, 9, 12 and 24 h) increased. Conclusion PA exposure can induce lipid deposition and HK-2 cells damage, and the mechanism may be related to PA-induced inflammatory response by activating NLRP3 inflammasome in HK-2 cells.