IL‑1β increases the expression of inflammatory factors in synovial fluid‑derived fibroblast‑like synoviocytes via activation of the NF‑κB‑mediated ERK‑STAT1 signaling pathway

作者：Jie Yang, Junhu Wang, Xiaojun Liang, Hongmou Zhao, Jun Lü, Qiang Ma, Bingfei Jing, Feng Tian · 发表于：Molecular Medicine Reports · 年份：2019 · DOI：10.3892/mmr.2019.10759 · 被引用次数：23 · 研究领域：Rheumatoid Arthritis Research and Therapies、Autoimmune and Inflammatory Disorders Research、Inflammasome and immune disorders

Interleukin (IL)‑1β serves a crucial role in the progression of rheumatoid arthritis. Previous studies have indicated that the ERK/STAT1 signaling pathway may be involved in the inflammatory response in synovial fluid‑derived fibroblast‑like synoviocytes (sfd‑FLSs). However, the molecular mechanisms underlying the pathological effects of the inflammatory factors induced by IL‑1β in sfd‑FLSs remain unclear. The aim of the present study was to investigate the IL‑1β‑mediated signaling pathways involved in the expression of inflammatory factors in sfd‑FLSs and in a rat model of rheumatoid arthritis. Reverse transcription‑quantitative PCR, western blotting, and immunohistochemistry were used to analyze the role of IL‑1β in the rat model of rheumatoid arthritis. The results suggested that IL‑1β administration exacerbated rheumatoid arthritis, bone injury and increased the expression levels of inflammatory factors, such as IL‑17 and tumor necrosis factor α (TNF‑α), whereas treatment with anti‑IL‑1β exhibited opposite effects. In vitro experiments in sfd‑FLSs further suggested that treatment with IL‑1β influenced the expression levels of various inflammatory factors. In specific, IL‑1β increased the expression of IL‑17 and TNF‑α, and decreased the expression of IL‑6 and IL‑10 in sfd‑FLSs. Additionally, treatment with IL‑1β increased the mRNA expression and protein phosphorylation of NF‑κB, ERK and STAT1 in sfd‑FLSs. Treatment with anti‑IL‑1β exhibited opposite effects on the expressi...