2-Acetylaminofluorene inhibits interleukin-1beta production in LPS-stimulated macrophages by blocking NF-kappaB/Rel activation

Cancer Lett. 2004 Jan 8;203(1):91-8. doi: 10.1016/j.canlet.2003.08.014.

Abstract

In the present study, we demonstrate the inhibitory effect of 2-acetylaminofluorene (AAF) on interleukin-1beta (IL-1beta) gene expression in lipopolysaccharide (LPS)-stimulated macrophages. Acetylaminofluorene inhibited IL-1 production in LPS-stimulated splenic macrophages and RAW 264.7 cells. Additionally, AAF also suppressed LPS-induced mRNA expression of IL-1beta in macrophages. To further characterize the molecular mechanism responsible for AAF-mediated suppression of IL-1beta, we investigated the effect of AAF on LPS-mediated activation of transcription factors, such as NF-kappaB, AP-1, CRE and NF-IL6, which are known to be important for LPS-induced gene expression of IL-1beta. Treatment of AAF caused a dose-related inhibition of LPS-induced NF-kappaB/Rel transcriptional activation, while the transcriptional activation of AP-1, CRE and NF-IL6 was not affected by AAF. Furthermore, LPS-induced NF-kappaB/Rel DNA binding was also suppressed by AAF treatment. These results suggest that AAF inhibits IL-1beta gene expression by blocking NF-kappaB/Rel activation.

MeSH terms

  • 2-Acetylaminofluorene / pharmacology*
  • Animals
  • Carcinogens / pharmacology*
  • Cell Line
  • Cells, Cultured
  • Enzyme Activation
  • Female
  • Gene Expression Regulation*
  • Genes, rel
  • Interleukin-1 / biosynthesis*
  • Lipopolysaccharides / pharmacology
  • Macrophage Activation / immunology*
  • Macrophages / drug effects*
  • Macrophages / immunology
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / biosynthesis*

Substances

  • Carcinogens
  • Interleukin-1
  • Lipopolysaccharides
  • NF-kappa B
  • 2-Acetylaminofluorene