TNF‑α increases inflammatory factor expression in synovial fibroblasts through the toll‑like receptor‑3‑mediated ERK/AKT signaling pathway in a mouse model of rheumatoid arthritis

Osteoarthritis is a type of joint disease that may lead to other joint diseases. Previous research has demonstrated that tumor necrosis factor (TNF)‑α is associated with osteoarthritis activity and pathology. The possible mechanisms of the TNF‑α‑mediated signaling pathway have not been clearly elaborated in synovial fibroblasts. The present study aimed to investigate the potential mechanisms of TNF‑α in a mouse model of iodoacetate‑induced osteoarthritis. Reverse transcription‑quantitative polymerase chain reaction, ELISA, western blotting and immunohistochemistry were performed to evaluate the role of TNF‑α in the progression of osteoarthritis. The results revealed that the serum levels of TNF‑α, interleukin (IL)‑1β, IL‑4 and IL‑6 were significantly upregulated in a mouse model of iodoacetate‑induced osteoarthritis compared with healthy mice (P