in MH7A cells established that its anti-RA activity was due to the modulation of the expression of Bax; Bcl-2; IL-6 and -8; MMP-1; MMP-2, -3, and -9; COX-2; and iNOS through the inhibition of the NF-kB and MAPK pathways [291]. This evidence concerns the gene PTGS2 and rheumatoid arthritis.