Polysaccharides from Acanthopanax senticosus enhances intestinal integrity through inhibiting TLR4/NF-κB signaling pathways in lipopolysaccharide-challenged mice

Anim Sci J. 2016 Aug;87(8):1011-8. doi: 10.1111/asj.12528. Epub 2015 Oct 5.

Abstract

To investigate the role of polysaccharide from Acanthopanax senticosus (ASPS) on lipopolysaccharide (LPS)-induced intestinal injury, mice in three treatments were administrated orally with or without ASPS (300 mg/kg body weight) for 14 days, followed by challenge with LPS or saline. At 4 h post-injection, blood and intestinal samples of six mice / treatment were collected. The results showed ASPS ameliorated LPS-induced intestinal morphological deterioration, proven by improved villus height (P < 0.05) and villus height : crypt depth ratio (P < 0.05). ASPS also elevated the mucosal barrier of LPS-challenged mice, supported by reduced plasma diamine oxidase (DAO) activity (P < 0.05) and L-lactate (P < 0.05), increased mucosal DAO activity (P < 0.05) as well as enhanced intestinal tight junction proteins expression involving occludin-1 (P < 0.05) and zonula occludens-1 (P < 0.05). In addition, ASPS decreased LPS-induced secretion of inflammatory mediators, including tumor necrosis factor (TNF)-α (P < 0.05) and prostaglandin E2 (P < 0.05). Also, ASPS down-regulated messenger RNA expression of toll-like receptor 4 (TLR4) and its downstream signals, including myeloid differentiation factor 88 (P < 0.05), TNF-α receptor-associated factor 6 (P < 0.05), as well as nuclear factor (NF)-κB p65 (P < 0.05) and its protein expression. These findings suggest that ASPS improves intestinal integrity under inflammation conditions connected with inhibiting TLR4/NF-κB signaling pathways.

Keywords: herbal extract; intestinal inflammation; metabolism; pro-inflammatory cytokines; toll-like receptor 4.

MeSH terms

  • Administration, Oral
  • Animals
  • Cytokines / metabolism
  • Depression, Chemical
  • Eleutherococcus / chemistry*
  • Escherichia coli
  • Inflammation
  • Inflammation Mediators / metabolism
  • Intestinal Diseases / chemically induced
  • Intestinal Diseases / drug therapy*
  • Intestinal Diseases / metabolism*
  • Intestinal Diseases / pathology
  • Lipopolysaccharides / adverse effects
  • Male
  • Mice, Inbred Strains
  • NF-kappa B / metabolism*
  • NF-kappa B / physiology
  • Phytotherapy*
  • Polysaccharides / administration & dosage*
  • Polysaccharides / isolation & purification
  • Polysaccharides / pharmacology*
  • Signal Transduction / drug effects*
  • Toll-Like Receptor 4 / metabolism*
  • Toll-Like Receptor 4 / physiology

Substances

  • Cytokines
  • Inflammation Mediators
  • Lipopolysaccharides
  • NF-kappa B
  • Polysaccharides
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4