Inhibition of NF-κB signaling pathway induces apoptosis and suppresses proliferation and angiogenesis of human fibroblast-like synovial cells in rheumatoid arthritis.

摘要: Background Rheumatoid arthritis (RA) is the most common inflammatory and a major cause of disability. The nuclear factor-kappa-light-chain-enhancer activated B cells (NF-κB) signaling pathway has been reported to be involved in pathogenesis RA with unclear mechanisms. Therefore, this study aims explore effect NF-κB on proliferation, apoptosis, angiogenesis human fibroblast-like synovial (HFLS) RA. Methods Normal HFLS RA-HFLS were selected as normal control groups, respectively. treated by BAY11-7082 (an inhibitor NF-κB) different concentrations, namely 2.5 μmol/L BAY11-7082, 5 μmol/LBAY11-7082 10 BAY11-7082. MTT assay was employed detect cell proliferation. Cell apoptosis determined flow cytometry at 24, 48, 72 hours after culture. Western blot analysis expressions NF-κB, angiogenesis-related factors (VEGF, Ang1, Ang2). Results Initially, we found that inhibited expression concentration-dependent manner. According findings cytometry, understood NF-κB), inhibition pathway, suppressed proliferation induced concentration time-dependent Furthermore, presented decreased VEGF, Ang1 Ang2 Conclusion concluded RA-HFLS, which could serve novel target treatment