Anti-malarial agent artesunate inhibits TNF-alpha-induced production of proinflammatory cytokines via inhibition of NF-kappaB and PI3 kinase/Akt signal pathway in human rheumatoid arthritis fibroblast-like synoviocytes

Rheumatology (Oxford). 2007 Jun;46(6):920-6. doi: 10.1093/rheumatology/kem014. Epub 2007 Feb 21.

Abstract

Objectives: Recent studies indicate that the anti-malarial agent artemisinin and its derivatives may exert an anti-inflammatory effect. In this study, we explored the effect of artesunate, an artemisinin derivative, on tumour necrosis factor (TNF)-alpha-induced production of interleukins, IL-1beta, IL-6 and IL-8, in human rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS), and further investigated the signal mechanism by which this compound modulates those cytokines' production.

Methods: RA FLS obtained from patients with active RA were stimulated with TNF-alpha and incubated with artesunate, and IL-1beta, IL-6 and IL-8 production was measured by ELISA. DNA-binding activity and nuclear translocation of nuclear factor kappa B (NF-kappaB) were measured by a sensitive multi-well colourimetric assay and confocal fluorescence microscopy, respectively. Signal transduction proteins expression was measured by western blot.

Results: Artesunate decreased the secretion of IL-1beta, IL-6 and IL-8 from TNF-alpha-stimulated RA FLS in a dose-dependent manner. Artesunate also prevented TNF-alpha-induced nuclear NF-kappaB translocation, DNA-binding activity and gene transcriptional activity, as well as phosphorylation and degradation of IkappaBalpha, but phosphorylation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase and c-Jun N-terminal kinase were unaffected. The production of IL-1beta, IL-6 and IL-8 induced by TNF-alpha was decreased by pyrrolidine dithiocarbamate (PDTC), a chemical inhibitor of NF-kappaB. These observations suggest that artesunate inhibits production of IL-1beta, IL-6 and IL-8 through inhibition of NF-kappaB signalling pathway. We also showed that artesunate prevented Akt phosphorylation. TNF-alpha-induced production of IL-1beta, IL-6 and IL-8 was hampered by treatment with the phosphatidylinositol 3 (PI3) kinase inhibitor LY294002, suggesting that inhibition of Akt activation might inhibit IL-1beta, IL-6 and IL-8 production induced by TNF-alpha.

Conclusions: Our results indicate that artesunate exerts an anti-inflammatory effect in RA FLS and provide the evidence that artesunate may have therapeutic potential for RA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Antimalarials / pharmacology*
  • Artemisinins / pharmacology*
  • Artesunate
  • Arthritis, Rheumatoid / metabolism
  • Arthritis, Rheumatoid / pathology*
  • Cells, Cultured
  • Cytokines / biosynthesis*
  • Dose-Response Relationship, Drug
  • Elafin / physiology
  • Female
  • Fibroblasts / drug effects
  • Fibroblasts / physiology
  • Genes, Reporter / drug effects
  • Humans
  • Inflammation Mediators / metabolism
  • Middle Aged
  • NF-kappa B / genetics
  • NF-kappa B / physiology
  • Sesquiterpenes / pharmacology*
  • Signal Transduction / drug effects
  • Synovial Membrane / drug effects
  • Synovial Membrane / metabolism
  • Synovial Membrane / pathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Antimalarials
  • Artemisinins
  • Cytokines
  • Elafin
  • Inflammation Mediators
  • NF-kappa B
  • PI3 protein, human
  • Sesquiterpenes
  • Tumor Necrosis Factor-alpha
  • Artesunate