Alcohol
Volume 30, Issue 1 , Pages 61-65, May 2003

Abamectin attenuates gastric mucosal damage induced by ethanol through activation of vagus nerve in rats

  • Ming-Yie Liu

      Affiliations

    • Graduate Institute of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan 704
    • Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan 704
    • Corresponding Author InformationCorresponding author. Graduate Institute of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan 704. Tel.: +886-2353535, ext. 5805; fax: +886-6-2752484
    • ,
  • James Po-Jung Chiang

      Affiliations

    • Graduate Institute of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan 704
    • ,
  • Dur-Zong Hsu

      Affiliations

    • Graduate Institute of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan 704
    • Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan 704
    • ,
  • Jou-Fang Deng

      Affiliations

    • Division of Clinical Toxicology, Department of Medicine, National Yang Ming University and Veterans General Hospital-Taipei, Taipei, Taiwan 112

Received 6 September 2002; received in revised form 16 April 2003; accepted 18 April 2003.

Editor: T.R. Jerrells

Abstract 

Some type A gamma-aminobutyric acid (GABAA) receptor agonists are effective in protecting against the formation of stomach lesions induced by ethanol. Natural product abamectin, one of the existing GABAA receptor agonists, might protect against the development of gastric ulcers induced by ethanol. We investigated the protective effect of abamectin against the formation of gastric mucosal lesions induced by ethanol in rats. Abamectin (3 mg/kg, p.o.) was given to rats 1 h before administration of ethanol [4 ml of a 30% (volume/volume) solution]. Mucosal lipid peroxidation (LPO), nitric oxide (NO) levels, and ulcer index were measured 3 h after gastric surgery (vagotomy vs. sham vagotomy) in treated versus control subjects. Abamectin attenuated ethanol-induced gastric ulceration, decreased LPO regeneration, and increased NO production in the gastric mucosa of rats in the sham vagotomy group. However, this protective effect of abamectin against ethanol-induced gastric lesions was not observed in rats in the group that underwent vagotomy. These results support the suggestion that administration of abamectin ameliorated the ethanol-induced gastric mucosal injury through elevation of NO production. Activation of the vagus nerve may be involved in the abamectin-associated gastric protection against the effects of ethanol in rats.

Keywords:  Ethanol, Abamectin, Lipid peroxidation, Nitric oxide, Vagus nerve

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PII: S0741-8329(03)00094-6

doi:10.1016/S0741-8329(03)00094-6

Alcohol
Volume 30, Issue 1 , Pages 61-65, May 2003

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