N-
methyl pyrrolidone (NMP), a small bioactive molecule, has the potential to stimulate bone formation and inhibit osteoclast differentiation. The aim of the present study was to investigate the effect of NMP on the inflammatory response and underlying molecular mechanisms in MG-63 cells. The
mRNA and
protein expression of
cytokines from peripheral blood in children with or without
ankle fracture were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and ELISA, respectively. MG-63 cells were pre-treated with/without NMP and stimulated with 1 µM
bradykinin (BK). The production of
cytokines from MG-63 cells was assessed by western blotting and RT-qPCR. The expression of
inducible nitric oxide synthase (iNOS) and
cyclooxygenase-2 (COX-2)
mRNA and
protein were measured using western blotting and/or RT-qPCR. Western blotting was used to examine the activation level of
mitogen activated protein kinase. Compared with healthy children, levels of
tumor necrosis factor (TNF-α),
interleukin (IL)-1β and
IL-6 mRNA and
protein were upregulated in children with
ankle fracture. NMP treatment did not induce cytotoxicity in MG-63 cells. The BK-induced upregulation of TNF-α, IL-1β,
IL-6, iNOS and COX-2
mRNA and
protein was reversed in a dose-dependent manner by NMP. Furthermore, NMP downregulated the activation of c-Jun NH2-terminal
kinase and p38 pathways, but not the extracellular signal-related
kinase pathway. Therefore, the results of the current study demonstrate that NMP inhibits
inflammation dependent on the
mitogen-activated protein kinase pathway in MG-63 cells, indicating that it may be beneficial in the healing of fractures.