Oligonol inhibits dextran sulfate sodium-induced colitis and colonic adenoma formation in mice

Antioxid Redox Signal. 2013 Jul 10;19(2):102-14. doi: 10.1089/ars.2012.4626. Epub 2013 May 15.

Abstract

Aims: To evaluate the effects of oligonol administration on experimentally induced colitis and colonic adenoma formation.

Results: Oral administration of oligonol protected against mouse colitis induced by dextran sulfate sodium (DSS). Under the same experimental conditions, oligonol administration significantly inhibited the activation of nuclear factor-kappa B and signal transducer and activator of transcription (STAT) 3 and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and cyclin D1 in the mouse colon. Further, oligonol inhibited azoxymethane-initiated and DSS-promoted adenoma formation in the mouse colon. Oligonol administration also attenuated lipid peroxidation (malondialdehyde) and protein oxidation (4-hydroxy-2-nonenal), thereby preventing oxidative stress-induced apoptosis of colonic epithelial cells. In vitro studies demonstrated that oligonol treatment reduced lipopolysaccharide-induced expression of interleukin (IL)-1β, tumor necrosis factor α, il-6, cox-2, and inos in murine macrophage RAW 264.7 cells. In another study, oligonol upregulated the antioxidant gene expression in the intestinal epithelial CCD841CoN cells and in the mouse colon.

Innovation: Oligonol, an innovative formulation of catechin-type oligomers derived from the lychee fruit extract, was tested in this study for the first time to evaluate its effects on experimentally induced colitis and colonic adenoma formation in mice.

Conclusion: Oligonol is effective in protecting against DSS-induced mouse colitis and colon carcinogenesis, suggesting that this polyphenol formulation may have a potential for the amelioration of inflammatory bowel disease and related disorders.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma / chemically induced
  • Adenoma / genetics
  • Adenoma / metabolism
  • Adenoma / prevention & control*
  • Animals
  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Carcinogenesis / drug effects
  • Carcinogenesis / genetics
  • Catechin / analogs & derivatives*
  • Catechin / pharmacology
  • Cell Line
  • Colitis / chemically induced
  • Colitis / genetics
  • Colitis / metabolism
  • Colitis / prevention & control*
  • Colonic Neoplasms / chemically induced
  • Colonic Neoplasms / genetics
  • Colonic Neoplasms / metabolism
  • Colonic Neoplasms / prevention & control*
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Dextran Sulfate
  • Humans
  • Inflammation / genetics
  • Inflammation / metabolism
  • Inflammation / prevention & control
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Lipid Peroxidation / drug effects
  • Lipid Peroxidation / genetics
  • Male
  • Mice
  • Mice, Inbred ICR
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Oxidative Stress / drug effects
  • Oxidative Stress / genetics
  • Phenols / pharmacology*
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antioxidants
  • Ccnd1 protein, mouse
  • Interleukin-1beta
  • NF-kappa B
  • Phenols
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tumor Necrosis Factor-alpha
  • oligonol
  • Cyclin D1
  • Catechin
  • Dextran Sulfate
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2