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)-??-induced　human　fibroblast-like　synoviocyte　rheumatoid　arthritis　(HFLS-RA)　cells,　and　its　associated　mechanisms.　After　TNF-??　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-??-induced　overexpression　of　MMPs　and　factors　associated　with　the　TLR4/NLRP3/NF-??B　pathway.　We　conclude　that　tectoridin　ameliorated　TNF-??-induced　proliferation　and　inflammation　by　inhibiting　TLR4/NLRP3/NF-??B　pathway.　It　might　provide　a　new　insight　for　the　clinical　application　of　RA.