Further validation using MH7A cells as a model revealed that the above components significantly inhibited cell proliferation and reduced the secretion of TNF-α-induced pro-inflammatory factors IL-6, IL-17A, and IL-1β, with a trend of action consistent with that of the total ARSHs, suggesting that the single components exerted their anti-RA effects by inhibiting synovial fibroblast activation and inflammatory factor release. The gene discussed is IL1B; the disease is rheumatoid arthritis.