Protective effect of δ-amyrone against ethanol-induced gastric ulcer in mice

Immunobiology. 2015 Jun;220(6):798-806. doi: 10.1016/j.imbio.2014.12.014. Epub 2014 Dec 30.

Abstract

The purpose of this study is to examine the protective effect of δ-amyrone on ethanol-induced gastric ulcer in mice. The mice intragastric administration 75% (0.5 mL/100g) ethanol was pretreated with δ-amyrone (4 and 8 mg/kg) and cimetidine (100 mg/kg) or vehicles in different experimental groups for a continuous three-day, and animals were euthanized 3h after ethanol ingestion. The gastric lesions were significantly attenuated by δ-amyrone (4 and 8 mg/kg) as compared to the ulcer control group. Pre-treatment with δ-amyrone prevented the myeloperoxidase (MPO) activity, production of nitric oxide (NO) in serum, expression of inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF-κB) p65 protein expression. Analysis of cytokines in gastric tissue and serum of ethanol-induced mice showed the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were decreased by δ-amyrone in response to NF-κB p65. These results suggested that δ-amyrone exerts its protective effect on experimental gastric ulcer by inhibiting NF-κB signaling pathways, which subsequently reduces overproduction of the inducible enzymes iNOS and suppresses the release of the inflammatory factors TNF-α, IL-6 and NO. Thus, δ-amyrone shows promise as a therapeutic agent in experimental gastric ulcer.

Keywords: Ethanol; Gastric ulcer; Inflammatory mediators; NF-κB; δ-Amyrone.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / biosynthesis
  • Cytokines / blood
  • Disease Models, Animal
  • Ethanol / adverse effects*
  • Gastric Acidity Determination
  • Gastric Mucosa / drug effects
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / pathology
  • Immunohistochemistry
  • Male
  • Mice
  • Mucus / metabolism
  • Nitric Oxide / blood
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Peroxidase / metabolism
  • Protective Agents / administration & dosage
  • Protective Agents / pharmacology*
  • Stomach Ulcer / chemically induced*
  • Stomach Ulcer / drug therapy
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / pathology*
  • Transcription Factor RelA / metabolism
  • Triterpenes / administration & dosage
  • Triterpenes / pharmacology*

Substances

  • Cytokines
  • Protective Agents
  • Transcription Factor RelA
  • Triterpenes
  • amyrone
  • Nitric Oxide
  • Ethanol
  • Peroxidase
  • Nitric Oxide Synthase Type II