Baicalein Inhibits Interleukin-1β-Induced Proliferation of Human Rheumatoid Arthritis Fibroblast-like Synoviocytes

Baicalein shows anti-inflammatory effects in human rheumatoid arthritis fibroblast-like synoviocytes (RAFLS). Considering its anti-proliferatory effects on various cancer cells, we investigated the effects of baicalein on interleukin-1 beta (IL-1 beta)-induced proliferation of human RAFLS. Cell proliferation was examined by H-3-thymidine incorporation assay. Western blot analysis was performed to assess the phosphorylation of extracellular regulating kinase (ERK), p38, and c-Jun N-terminal kinase, and nuclear translocation of nuclear factor kappa B (NF-kappa B) subunit p65. Notably, baicalein significantly suppressed IL-1 beta-mediated RAFLS proliferation (P < 0.05), along with reduced ERK1/2 and p38 phosphorylation. The IL-1 beta-induced p65 nuclear translocation and NF-kappa B DNA binding activity was significantly decreased by baicalein. Additionally, the inhibitory effects of baicalein on IL-1 beta-induced proliferation of RAFLS were dose-dependently reversed by the addition of recombinant macrophage migration inhibitory factory (MIF). Our results indicate that baicalein inhibits IL-1 beta-induced RAFLS proliferation, which involves suppression of NF-kappa B transcriptional activity and MIF-mediated signaling.