Sulfated chitosan oligosaccharides suppress LPS-induced NO production via JNK and NF-κB inactivation

Molecules. 2014 Nov 7;19(11):18232-47. doi: 10.3390/molecules191118232.

Abstract

Various biological effects have been reported for sulfated chitosan oligosaccharides, but the molecular mechanisms of action of their anti-inflammatory effects are still unknown. This study aimed to evaluate the anti-inflammatory effects of sulfated chitosan oligosaccharides and to elucidate the possible mechanisms of action. The results showed that pretreated low molecular weight sulfated chitosan oligosaccharides inhibited the production of nitric oxide (NO) and inflammatory cytokines such as IL-6 and TNF-α in lipopolysaccharide (LPS)-activated RAW264.7 cells. The sulfated chitosan oligosaccharides also suppressed inducible nitric oxide synthase (iNOS), phosphorylation of JNK and translocation of p65, a subunit of NF-κB, into the nucleus by inhibiting degradation of IκB-α. Our investigation suggests sulfated chitosan oligosaccharides inhibit IL-6/TNF-α in LPS-induced macrophages, regulated by mitogen-activated protein kinases (MAPKs) pathways dependent on NF-κB activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Chitosan / chemistry*
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / toxicity*
  • MAP Kinase Kinase 4 / metabolism*
  • MAP Kinase Signaling System / drug effects
  • Macrophages / metabolism*
  • Macrophages / pathology
  • Mice
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type II / biosynthesis
  • Oligosaccharides / chemistry
  • Oligosaccharides / pharmacology*
  • Transcription Factor RelA / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • Oligosaccharides
  • Rela protein, mouse
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Chitosan
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • MAP Kinase Kinase 4