Rhodojaponin Ii Inhibits Tnf-Alpha-Induced Inflammatory Cytokine Secretion In Mh7a Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes

Rhodojaponin II (R-II) has been shown to possess anti-inflammatory activity. Herein, we aimed to explore the effect of R-II on tumor necrosis factor-alpha (TNF-alpha)-induced inflammation in MH7A rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs). We found that R-II treatment at high concentration suppressed the viability of MH7A cells. R-II suppressed the levels of nitric oxide and prostaglandin E2, and inhibited messenger RNA expression and concentrations of interleukin-1 beta (IL-1 beta), IL-6 and matrix metalloproteinase-1 in TNF-alpha-stimulated RA-FLSs. Additionally, R-II repressed TNF-alpha-induced activation of the Akt, nuclear factor-kappa B (NF-kappa B), and toll-like receptor 4 (TLR4)/MyD88 pathways in MH7A cells. Inhibition of the Akt, NF-kappa B, and TLR4/MyD88 pathways by the corresponding inhibitors reinforced the inhibitory effect of R-II on TNF-alpha-induced inflammatory cytokine secretion in MH7A cells. R-II ameliorated the severity of collagen-induced arthritis in mice by inhibiting inflammation. In conclusion, R-II repressed TNF-alpha-induced inflammatory response in MH7A cells by inactivating the Akt, NF-kappa B, and TLR4/MyD88 pathways.