In summary, RES regulates the activation of the SIRT1/NF-κB/miR-29a-3p/Keap1 pathway and the SIRT1/NF-κB/miR-23a-3p/cul3 pathway, subsequently activating the Nrf2-ARE signaling pathway, effectively inhibiting oxidative stress resulting from ROS accumulation and mitigating joint inflammation, positioning it as a promising candidate drug for RA prevention and treatment. This evidence concerns the gene NFKB1 and rheumatoid arthritis.