Effect of diallyl disulfide on acute gastric mucosal damage induced by alcohol in rats

Hum Exp Toxicol. 2015 Mar;34(3):227-39. doi: 10.1177/0960327114537095. Epub 2014 Jun 27.

Abstract

This study investigated the gastroprotective effects of diallyl disulfide (DADS), a secondary organosulfur compound derived from garlic (Allium sativum L.) on experimental model of ethanol (EtOH)-induced gastric ulcer in rats. The antiulcerogenic activity of DADS was evaluated by gross/histopathological inspection, pro-inflammatory cytokines, and lipid peroxidation with antioxidant enzyme activities in the stomach. DADS (100 mg/kg) was administered by oral gavage 2 h prior to EtOH treatment (5 ml/kg). The animals were killed 1 h after receiving EtOH treatment. Pretreatment with DADS attenuated EtOH-induced gastric mucosal injury, as evidenced by decreased severity of hemorrhagic lesions and gastric ulcer index upon visual inspection. DADS also prevented histopathological alterations and gastric apoptotic changes caused by EtOH. An increase in tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase was observed in the gastric tissues of EtOH-treated rats that coincided with increased serum TNF-α and interleukin 6 levels. In contrast, DADS effectively suppressed production of pro-inflammatory mediators induced by EtOH. Furthermore, DADS prevented the formation of gastric malondialdehyde and the depletion of reduced glutathione content and restored antioxidant enzyme activities, such as catalase, glutathione peroxidase, and glutathione reductase in the gastric tissues of EtOH-treated rats. These results indicate that DADS prevents gastric mucosal damage induced by acute EtOH administration in rats and that the protective effects of DADS may be due to its potent antioxidant and anti-inflammatory activities.

Keywords: Ethanol; diallyl disulfide; gastric mucosal damages; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allyl Compounds / pharmacology
  • Allyl Compounds / therapeutic use*
  • Animals
  • Anti-Ulcer Agents / pharmacology
  • Anti-Ulcer Agents / therapeutic use*
  • Apoptosis / drug effects
  • Catalase / metabolism
  • Disulfides / pharmacology
  • Disulfides / therapeutic use*
  • Ethanol
  • Female
  • Gastric Mucosa / drug effects
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / pathology
  • Glutathione / metabolism
  • Glutathione Peroxidase / metabolism
  • Glutathione Reductase / metabolism
  • Interleukin-6 / blood
  • Interleukin-6 / metabolism
  • Nitric Oxide Synthase Type II / blood
  • Nitric Oxide Synthase Type II / metabolism
  • Rats, Sprague-Dawley
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / drug therapy*
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / pathology
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Allyl Compounds
  • Anti-Ulcer Agents
  • Disulfides
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Ethanol
  • diallyl disulfide
  • Catalase
  • Glutathione Peroxidase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat
  • Glutathione Reductase
  • Glutathione