[No authors listed]
Interleukin (IL)â1β serves a crucial role in the progression of rheumatoid arthritis. Previous studies have indicated that the signaling pathway may be involved in the inflammatory response in synovial fluidâderived fibroblastâlike synoviocytes (sfdâFLSs). However, the molecular mechanisms underlying the pathological effects of the inflammatory factors induced by ILâ1β in sfdâFLSs remain unclear. The aim of the present study was to investigate the ILâ1βâmediated signaling pathways involved in the expression of inflammatory factors in sfdâFLSs and in a rat model of rheumatoid arthritis. Reverse transcriptionâquantitative PCR, western blotting, and immunohistochemistry were used to analyze the role of ILâ1β in the rat model of rheumatoid arthritis. The results suggested that ILâ1β administration exacerbated rheumatoid arthritis, bone injury and increased the expression levels of inflammatory factors, such as ILâ17 and tumor necrosis factor α (TNFâα), whereas treatment with antiâILâ1β exhibited opposite effects. In vitro experiments in sfdâFLSs further suggested that treatment with ILâ1β influenced the expression levels of various inflammatory factors. In specific, ILâ1β increased the expression of ILâ17 and TNFâα, and decreased the expression of ILâ6 and ILâ10 in sfdâFLSs. Additionally, treatment with ILâ1β increased the mRNA expression and protein phosphorylation of NFâκB, ERK and in sfdâFLSs. Treatment with antiâILâ1β exhibited opposite effects on the expression levels of inflammatory factors and suppressed the NFâκBâmediated signaling pathway activation in sfdâFLSs. Finally, treatment with a NFâκB inhibitor suppressed the effects of ILâ1β, and NFâκB overexpression reversed the effects of antiâILâ1β on the expression levels of ILâ17, TNFâα, NFâκB, ERK and In conclusion, the present results demonstrated that treatment with ILâ1β increased the expression levels of inflammatory factors in sfdâFLSs via the regulation of the NFâκBâmediated ERK/duanyu18131 signaling pathway in a rat model of rheumatoid arthritis. Therefore, the signaling pathway may represent a potential target for the development of novel treatments for rheumatoid arthritis.
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