Lunasin and lunasin-like peptides inhibit inflammation through suppression of NF-kappaB pathway in the macrophage

Peptides. 2009 Dec;30(12):2388-98. doi: 10.1016/j.peptides.2009.08.005. Epub 2009 Aug 12.

Abstract

Inflammation is part of the host defense mechanism against harmful matters and injury; however, aberrant inflammation is associated to the development of chronic diseases such as cancer. Lunasin is a novel peptide that demonstrates potential anticancer activity against mammalian cancer cell lines and may play a role in inflammation. The objective of this study was to determine the mechanism of action by which lunasin and lunasin-like peptides exert their anti-inflammatory properties using RAW 264.7 macrophage cell line as an in vitro model. We purified three peptides (5, 8, and 14 kDa) from defatted soybean flour with a positive immunoreactivity towards lunasin mouse monoclonal antibody. Treatment with these peptides (10-50 microM) resulted in the inhibition of pro-inflammatory markers in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. The 5 kDa peptide inhibited most potently pro-inflammatory markers including interleukin-6 production (IC(50)=2 microM), interleukin-1beta production (IC(50)=13 microM), nuclear factor-kappa B (NF-kappaB) transactivation (IC(50)=21 microM), cyclooxygenase-2 expression (IC(50)=25 microM), nitric oxide production (IC(50)=28 microM), inducible nitric oxide synthase expression (IC(50)=37 microM), prostaglandin E(2) production (IC(50)=41 microM), p65 nuclear translocation (IC(50)=48 microM) and p50 nuclear translocation (IC(50)=77 microM). In conclusion, lunasin and lunasin-like peptides purified from defatted soybean flour inhibited inflammation in LPS-induced RAW 264.7 macrophage by suppressing NF-kappaB pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Blotting, Western
  • Cell Line, Tumor
  • Cyclooxygenase 1 / metabolism
  • Cyclooxygenase 2 / metabolism
  • Dinoprostone / metabolism
  • Inflammation / chemically induced
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology
  • Macrophages / drug effects*
  • Macrophages / immunology*
  • Membrane Proteins / metabolism
  • Mice
  • NF-kappa B / metabolism*
  • Nitric Oxide Synthase Type II / metabolism
  • Peptides / chemistry
  • Peptides / pharmacology*
  • Signal Transduction / drug effects*
  • Soybean Proteins / pharmacology*

Substances

  • Anti-Inflammatory Agents
  • GM2S-1 protein, Glycine max
  • Interleukin-6
  • Lipopolysaccharides
  • Membrane Proteins
  • NF-kappa B
  • Peptides
  • Soybean Proteins
  • Nitric Oxide Synthase Type II
  • Ptgs2 protein, mouse
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Ptgs1 protein, mouse
  • Dinoprostone