Enhancement of gastric mucosal integrity by Lactobacillus rhamnosus GG

Life Sci. 2007 May 16;80(23):2128-2136. doi: 10.1016/j.lfs.2007.03.018. Epub 2007 Apr 18.

Abstract

The gastric mucosa is frequently exposed to different exogenous and endogenous ulcerative agents. Alcoholism is one of the risk factors for the development of mucosal damage in the stomach. This study aimed to assess if a probiotic strain Lactobacillus rhamnosus GG (LGG) is capable of protecting the gastric mucosa from acute damage induced by intragastric administration of ethanol. Pre-treatment of rats with LGG at 10(9) cfu/ml twice daily for three consecutive days markedly reduced ethanol-induced mucosal lesion area by 45%. LGG pre-treatment also significantly increased the basal mucosal prostaglandin E(2) (PGE(2)) level. In addition, LGG attenuated the suppressive actions of ethanol on mucus-secreting layer and transmucosal resistance and reduced cellular apoptosis in the gastric mucosa. It is suggested that the protective action of LGG on ethanol-induced gastric mucosal lesions is likely attributed to the up-regulation of PGE(2), which could stimulate the mucus secretion and increase the transmucosal resistance in the gastric mucosa. All these would protect mucosal cells from apoptosis in the stomach.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Dinoprostone / metabolism
  • Ethanol / chemistry
  • Ethanol / pharmacology
  • Gastric Mucosa / metabolism*
  • Gastric Mucosa / pathology*
  • Lactobacillus rhamnosus / metabolism*
  • Male
  • Mucin-6
  • Mucins / biosynthesis
  • Mucous Membrane / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Up-Regulation

Substances

  • Muc6 protein, rat
  • Mucin-6
  • Mucins
  • RNA, Messenger
  • Ethanol
  • Dinoprostone