BACKGROUND The present study aimed to investigate the potential effects of propofol on ankle fracture healing in children and the underlying molecular mechanisms. MATERIAL AND METHODS We first detected the levels of inflammatory cytokines from peripheral blood in children with or without ankle fracture using quantitative real-time polymerase chain reaction (qRT-PCR) and ELISA assay. Then, effects of propofol on inflammatory response in MG-63 cells were investigated. MG-63 cells were pre-treated with or without propofol and then stimulated with 1 μM bradykinin (BK). The productions of cytokines from MG-63 cells were determined by using qRT-PCR and Western blot assay. The expression levels of p-p38, NF-κB p-p65, NLRP3, ASC, caspase-1, and COX-2 were measured by Western blot and/or qRT-PCR. RESULTS The results showed that, compared with the healthy children, the levels of tumor necrosis factor (TNF-α), interleukin (IL)-1β, and IL-6 were significantly up-regulated in children with fractured ankles. No cytotoxicity was observed in MG-63 cells after propofol treatment. BK treatment significantly enhanced TNF-α, IL-1β, and IL-6 expression levels, and these enhancements were reduced by propofol treatment in a dose-dependent manner. Moreover, BK-induced up-regulation of p-p38, NF-κB p-p65, NLRP3, ASC, caspase-1, and COX-2 was dose-dependently down-regulated by propofol treatment. CONCLUSIONS Propofol prevents inflammation in MG-63 cells by regulating p38MAPK-NF-κB pathway, NLRP3 inflammasome, and COX-2 expression. Our findings indicate the benefits of propofol in fracture healing, and provide a more theoretical basis for the clinical treatment of fractures.