Malloapelta B suppresses LPS-induced NF-κB activation and NF-κB-regulated target gene products

Int Immunopharmacol. 2015 Feb;24(2):147-152. doi: 10.1016/j.intimp.2014.12.008. Epub 2014 Dec 12.

Abstract

Nuclear factor-κB (NF-κB) and the signaling pathways that regulate its activity have become a focal point for intense drug research and development efforts. NF-κB regulates the transcription of a large number of genes, particularly those involved in immune, inflammatory, and anti-apoptotic responses. In our search for NF-κB inhibitors from natural resources, we identified malloapelta B as an inhibitor of NF-κB activation from Mallotus apelta Muell-Arg. In the present study, we demonstrated the effect of malloapelta B on NF-κB activation in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. This compound suppressed NF-κB activation through the inhibition of IκB kinase (IKK) activation, thereby blocking the phosphorylation and degradation of the inhibitor of NF-κB alpha (IκBα), and the nuclear translocation and DNA-binding activity of p65. The suppression of NF-κB by malloapelta B led to the down-regulation of target genes involved in inflammation and proliferation. Taken together, this study extends our understanding on the mechanisms underlying the possible anti-inflammatory and anti-cancer activities of malloapelta B. Our findings provide new insight into its mechanisms of action and propose a potential application of malloapelta B for inflammatory diseases as well as certain cancers associated with abnormal NF-κB activation.

Keywords: Inflammation; IκBα; Malloapelta B; Nuclear factor-κB (NF-κB); Proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzopyrans / isolation & purification
  • Benzopyrans / pharmacology*
  • Cell Line
  • Cell Nucleus / metabolism*
  • Cell Proliferation / genetics
  • Inflammation / genetics
  • Lipopolysaccharides / immunology
  • Macrophages / drug effects*
  • Macrophages / immunology
  • Mallotus Plant / immunology
  • Mice
  • NF-kappa B / metabolism*
  • Phosphorylation / drug effects
  • Protein Transport
  • Transcription Factor RelA / metabolism*
  • Transcriptional Activation / drug effects

Substances

  • Benzopyrans
  • Lipopolysaccharides
  • NF-kappa B
  • Rela protein, mouse
  • Transcription Factor RelA
  • malloapelta B