Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Int J Mol Sci. 2016 Sep 1;17(9):1455. doi: 10.3390/ijms17091455.

Abstract

Previous studies have shown that ghrelin reduces colonic inflammation induced by trinitrobenzene sulfonic acid and dextran sodium sulfate. In the present study we determined the effect of treatment with ghrelin on the course of acetic acid-induced colitis in rats. Rectal administration of 3% acetic acid solution led to induction of colitis in all animals. Damage of the colonic wall was accompanied by an increase in mucosal concentration of pro-inflammatory interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), as well mucosal activity of myeloperoxidase. Moreover, induction of colitis led to a reduction in colonic blood flow and DNA synthesis. Administration of ghrelin after induction of colitis led to faster regeneration of the colonic wall and reduction in colonic levels of IL-1β, TNF-α, and myeloperoxidase. In addition, treatment with ghrelin improved mucosal DNA synthesis and blood flow. Our study disclosed that ghrelin exhibits a strong anti-inflammatory and healing effect in acetic acid-induced colitis. Our current observation in association with previous findings that ghrelin exhibits curative effect in trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis suggest that therapeutic effect of ghrelin in the colon is universal and independent of the primary cause of colitis.

Keywords: DNA synthesis; colitis; interleukin-1β; mucosal blood flow; myeloperoxidase.

MeSH terms

  • Acetic Acid / toxicity
  • Animals
  • Colitis, Ulcerative / drug therapy*
  • Colitis, Ulcerative / etiology
  • DNA / biosynthesis
  • Ghrelin / administration & dosage
  • Ghrelin / pharmacology
  • Ghrelin / therapeutic use*
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Male
  • Peroxidase / metabolism
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Ghrelin
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • DNA
  • Peroxidase
  • Acetic Acid