LA showed anti-inflammation activity on IL-1β-stimulated mouse chondrocytes in arthritis models by a complex mechanism involving inhibition of phosphorylation of NF-κBp65 and IκBαn, decreasing the production of PGE2 and NO, and downregulating the expression of iNOS, COX-2, ADAMTS, MMP1, MMP3, and MMP13 by blocking NF-κB and wnt/β-catenin signaling (Chen WP. Here, NFKB1 is linked to arthritic joint disease.