NFKB1 and rheumatoid arthritis: These results demonstrated that the HP@CEL could effectively mediate the cross-talk of macrophages and synovial fibroblasts through inhibiting the M1 phonotype macrophages and the proliferation of synovial fibroblasts by down-regulating TLR4/NF-κB signaling pathway, leading to a lower level of proinflammatory cytokines, which hold potential for relieving the chronic inflammation and blocking the progression of RA.