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Rheumatoid arthritis (RA) severely affects the quality life of patients due to its high association with disability. Traditional Chinese medicines have been reported to exert notable therapeutic effects on RA. The Chinese medicinal prescription Wang‑Bi Tablet (WB) has been successfully used to clinically treat RA for many years; however, its pharmacological mechanism of action is largely unclear. In the present study, adjuvant‑induced arthritis (AIA) rats were used to evaluate the anti‑inflammatory effects of WB and western blotting was used to explore the molecular mechanisms. The experimental results demonstrated that WB treatment significantly reduced arthritis score and hind‑paw volume. Furthermore, synovial hyperplasia, inflammatory cell infiltration and joint destruction were ameliorated by WB. The expression levels of the proinflammatory cytokines interleukin (IL)‑1β, tumor necrosis factor‑α and IL‑6, were reduced in the joints of WB‑treated rats. Western blotting revealed that WB could also inhibit excessive activation of nuclear factor (NF)‑κB and Janus kinase (JAK)‑signal transducer and activator of transcription 3 (STAT3) signaling pathways. These results indicated that the therapeutic effects of WB on AIA may be accomplished through inhibition of the NF‑κB and JAK‑STAT3 signaling pathways. These findings provide experimental evidence to support WB as a therapeutic agent for the treatment of patients with RA.

Suppressive effects of Wang‑Bi Tablet on adjuvant‑induced arthritis in rats via NF‑κB and STAT3 signaling pathways