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Inflammation. 2014 Feb;37(1):163-9. doi: 10.1007/s10753-013-9725-9.

Baicalein inhibits interleukin-1β-induced proliferation of human rheumatoid arthritis fibroblast-like synoviocytes.

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  • 1Department of Orthopedics, The 97th Hospital of PLA, Xuzhou, 221004, Jiangsu, China.

Abstract

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-1β)-induced proliferation of human RAFLS. Cell proliferation was examined by (3)H-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-κB) subunit p65. Notably, baicalein significantly suppressed IL-1β-mediated RAFLS proliferation (P < 0.05), along with reduced ERK1/2 and p38 phosphorylation. The IL-1β-induced p65 nuclear translocation and NF-κB DNA binding activity was significantly decreased by baicalein. Additionally, the inhibitory effects of baicalein on IL-1β-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-1β-induced RAFLS proliferation, which involves suppression of NF-κB transcriptional activity and MIF-mediated signaling.

PMID:
24005900
[PubMed - indexed for MEDLINE]
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