Compared with the IL-23 overexpression model group, XTS significantly decreased the expression levels of IL-23 and IL-17 in a dose-dependent manner and inhibited the phosphorylation of NF-κB (P < 0.01), indicating that XTS can suppress the IL-23/IL-17/NF-κB inflammatory axis in IL-23 overexpressing RAFLS cells, thereby inhibiting synovial inflammation in RA. Here, NFKB1 is linked to rheumatoid arthritis.