Activated NF‐κB signalling pathway in OA‐FLS inflammation. CTGF promoted the generation of IL‐6 in human OA‐FLS through the ανβ5 integrin, ASK1, p38/JNK and AP‐1/NF‐kB signal transduction pathways. CTGF‐induced IL‐β in human OA‐FLS through αvβ3/ανβ5 integrins, ROS, and ASK1, p38/JNK, and NF‐κB signal transduction pathways, which attenuated by berberine, an anti‐inflammatory isoquinoline alkaloid separated from the Chinese herb Rhizoma coptidis (Huang Lian). CTGF enhanced MCP‐1 production in human OA‐FLS through the ανβ5 integrin, FAK, MEK, ERK and NF‐κB/AP‐1 signalling pathway. FSLT1 elevated TNF‐α, IL‐1β and IL‐6 generation in human OA‐FLS via activated NF‐κB signalling pathway. FSLT1 increased OA‐FLS proliferation by down‐regulating p53 and p21. Moreover, p21 was reported to block the elevated IL‐6 and MMPs, participated in the development of OA. WY‐14643, an agonist of PPAR‐α, decreased LPS‐induced NO, PGE2, inflammatory mediators (VCAM‐1, ICAM‐1, ET‐1 and TF), and pro‐inflammatory cytokines (IL‐6, IL‐1β, TNF‐α and MCP‐1) production in human OA‐FLS by suppressing LPS‐mediated NF‐κB activation and IkB phosphorylation. p53, a tumour‐suppressor protein. p21, a cyclin‐dependent kinase inhibitor