The present results revealed that PF could effectively improve collagen-induced RA in rats by inhibiting Rho kinase activation in the joint synovial tissues, in turn down-regulating expression of p-NF-κB p65 and reducing contents of pro-inflammatory cytokines.
Accordingly, attenuating p65-mediated production of IL-1β and TNFα by blocking the citrullination of p65 has great therapeutic potential in rheumatoid arthritis.
In conclusion, our paper strongly demonstrated the protective effect of rutin against the rheumatoid arthritis involved via suppression of NF-κB p65 protein expression.
Expression of TLR4, PU.1, NF-κB p65 and IκBα on synovial fluid macrophages from RA patients was determined by Western blotting, and cytokines were measured by ELISA.
Immunohistochemistry for TNFAIP3, NF-kB p65 and phosphorylated NF-kB p65 protein expression was performed in 6 RA knee joint synovium samples compared to 9 osteoarthritis (OA) samples.
In sharp contrast, DEX did not affect TNFalpha-induced IKK phosphorylation, IkappaBalpha degradation, p65 nuclear translocation, or MAPK activation in RA FLS.
Moreover, analyses confirm the presence of CREB-1 and NF-kappaB p50 and p65 subunit binding to the NURR1 promoter under basal conditions in freshly explanted RA synovial tissue.