ABSTRACT Fibroblast‐like synoviocytes (FLS) drive rheumatoid arthritis (RA) progression. Bacopaside I (BSI), a major component of the anti‐RA herb Bacopa monnieri , demonstrates anti‐arthritic effects in RA animal models; however, its precise anti‐rheumatic mechanisms, especially regarding suppression of RA‐FLS pathogenicity, remain unclear. Collagen‐induced arthritis (CIA) rats and TNF‐α‐stimulated RA‐FLS were used as in vivo and in vitro models of RA. We studied BSI's therapeutic potential in CIA rats and its influences on TNF‐α‐induced migration, invasion, and inflammation in RA‐FLS, focusing on the underlying mechanism of Wnt/β‐catenin pathway inhibition. BSI exhibited arthritis‐alleviating activity in CIA rats, as evidenced by reductions in paw swelling, arthritis index, and histological damage to ankle joints. It also decreased serum and synovial levels of IL‐1β, IL‐6, and TNF‐α, indicating anti‐inflammatory effects in vivo. At non‐cytotoxic concentrations, BSI inhibited migration, invasion, and F‐actin remodeling in TNF‐α‐stimulated RA‐FLS. Similar to its anti‐inflammatory activity in vivo, BSI decreased pro‐inflammatory factor production in vitro, including IL‐1β, IL‐6, IL‐8, MMP‐2, and MMP‐9. Mechanistically, BSI treatment inhibited Wnt/β‐catenin pathway activation in both CIA rat synovium and TNF‐α‐stimulated RA‐FLS, as demonstrated by decreased Wnt1, p‐GSK‐3β (Ser9), and β‐catenin protein levels, increased p‐β‐catenin, reduced β‐catenin nuclear translocation, and a lower TOP/FOP ratio. Importantly, the critical involvement of this pathway was further confirmed by the loss of BSI's benefits following β‐catenin overexpression in TNF‐α‐stimulated RA‐FLS. BSI ameliorates arthritis severity and RA‐FLS pathogenicity by suppressing the Wnt/β‐catenin pathway, highlighting its promise as a novel candidate for RA treatment.