SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway

摘要: Rheumatoid arthritis (RA) is an autoimmune disease of the joints characterized by synovial hyperplasia and chronic inflammation. Fibroblast-like synoviocytes (FLS) play a central role in RA initiation, progression, perpetuation. Prior studies showed that sirtuin 1 (SIRT1), deacetylase participating broad range transcriptional metabolic regulations, may impact cell proliferation inflammatory responses. However, SIRT1 RA-FLS was unclear. Here, we explored effects on aggressiveness responses cultured RA-FLS. expression significantly lower tissues FLS from patients than healthy controls. Overexpression inhibited proliferation, migration, invasion. overexpression also increased apoptosis caspase-3 -8 activity. Focusing phenotypes, found reduced secretion TNF-α, IL-6, IL-8, IL-1β. Mechanistic further revealed suppressed NF-κB pathway reducing p65 protein expression, phosphorylation, acetylation Our results suggest key regulator pathogenesis suppressing aggressive phenotypes response FLS. Enhancing or function could be therapeutic beneficial for inhibiting