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

Ming Yie Liu, James Po Jung Chiang, Dur Zong Hsu, Jou Fang Deng

研究成果: Article同行評審

11 引文 斯高帕斯(Scopus)

摘要

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.

原文English
頁(從 - 到)61-65
頁數5
期刊Alcohol
30
發行號1
DOIs
出版狀態Published - 2003 5月

All Science Journal Classification (ASJC) codes

  • 健康(社會科學)
  • 生物化學
  • 毒理學
  • 神經內科
  • 行為神經科學

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