Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by
inflammation infiltration of the synovial tissues and the fibroblast-like synoviocytes.
Tectoridin is a botanical active ingredient with anti-inflammatory properties. In this study, the anti-arthritic effects of
tectoridin and its mechanism of action are examined in TNF-α-induced human fibroblast-like synovial cells (HFLSs cells) and complete
Freund's adjuvant (CFA)-stimulated arthritic mice.
Arthritis progression was evaluated via bodyweight, hind paw swelling, organ index, and synovial pathology. IL-1β,
IL-6 and other pro-inflammatory factors concentrations, and the expression of MAPK pathway
proteins in HFLSs cells and arthritic mice were measured using ELISA and western blotting. Results showed that
tectoridin significantly decreased the swelling of the paws and joints as well as the increased immune organ index within CFA-induced arthritic mice. Histopathological analysis showed that
tectoridin alleviated the lesions of ankle joints and synovial tissues induced by CFA. Secretion of pro-inflammatory
cytokines in TNF-α-induced HFLSs cells and CFA-stimulated arthritic mice were also abated by
tectoridin. Similarly, the presence of
tectoridin significantly inhibited the abnormal phosphorylation levels of ERK, JNK, and p38 in vivo and in vitro. All those results highlighted that
tectoridin exhibits anti-
arthritis effects by inhibiting MAPK-mediated inflammatory responses.