Tectoridin ameliorates proliferation and inflammation in TNF-α-induced HFLS-RA cells via suppressing the TLR4/NLRP3/NF-κB signaling pathway

Tectoridin, isolated from the dry rhizome of iris, is a compound with multiple biological activities. However, its biological roles in rheumatoid arthritis (RA) have still not been clearly elucidated. The aim of this study was to focus on the effects of tectoridin on tumor necrosis factor (TNF)-α-induced human fibroblast‑like synoviocyte rheumatoid arthritis (HFLS‑RA) cells, and its associated mechanisms. After TNF-α stimulation, CCK8 and MTT assays, TUNEL assay and flow cytometry, Western blotting and immunohistochemistry analysis were performed to check the cell proliferation, cell apoptosis and cycle analysis, and the expression of related proteins, respectively. Our results showed that tectoridin significantly hindered cell proliferation, S-to-G2/M phase transition and down-regulated Cyclind 1 and PCNA protein levels. Additionally, tectoridin markedly promoted apoptosis rates of HFSL-RA cells and elevated the expression levels of Cleaved Caspase-3 and Bax, while reduced the expression level of Bcl-2. Moreover, tectoridin reversed TNF-α-induced overexpression of MMPs and factors associated with the TLR4/NLRP3/NF-κB pathway. We conclude that tectoridin ameliorated TNF-α-induced proliferation and inflammation by inhibiting TLR4/NLRP3/NF-κB pathway. It might provide a new insight for the clinical application of RA.