Abstract

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.

Keywords: ankle fractures, Propofol