Potential protective effects of Clostridium butyricum on experimental gastric ulcers in mice

World J Gastroenterol. 2015 Jul 21;21(27):8340-51. doi: 10.3748/wjg.v21.i27.8340.

Abstract

Aim: To investigate the effects of Clostridium butyricum (C. butyricum) on experimental gastric ulcers (GUs) induced by alcohol, restraint cold stress, or pyloric ligation in mice, respectively.

Methods: One hundred and twenty mice were randomly allocated into three types of gastric ulcer models (n = 40 each), induced by alcohol, restraint cold stress, or pyloric ligation. In each GU model, 40 mice were allocated into four groups (n = 10 each): the sham control group; model group (GU induction without pretreatment); C. butyricum group (GU induction with C. butyricum pretreatment); and Omeprazole group (GU induction with Omeprazole pretreatment). The effects of C. butyricum were evaluated by examining the histological changes in the gastric mucosal erosion area, the activities of superoxide dismutase (SOD) and catalase (CAT), the level of malondialdehyde (MDA), and the contents of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, leukotriene B4 (LTB4) and 6-keto-PGF-1α (degradation product of PGI2) in the gastric tissue.

Results: Our data showed that C. butyricum significantly reduced the gastric mucosal injury area and ameliorated the pathological conditions of the gastric mucosa. C. butyricum not only minimized the decreases in activity of SOD and CAT, but also reduced the level of MDA in all three GU models used in this study. The accumulation of IL1-β, TNF-α and LBT4 decreased, while 6-keto-PGF-1α increased with pretreatment by C. butyricum in all three GU models.

Conclusion: Our data demonstrated the protective effects of pretreatment with C. butyricum on anti-oxidation and anti-inflammation in different types of GU models in mice. Further studies are needed to explore its potential clinical benefits.

Keywords: Clostridium butyricum; Gastric ulcer; Inflammation; Oxidative stress; Probiotics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / metabolism
  • Animals
  • Catalase / metabolism
  • Clostridium butyricum / physiology*
  • Cold Temperature
  • Disease Models, Animal
  • Ethanol
  • Gastric Mucosa / drug effects
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / microbiology*
  • Gastric Mucosa / pathology
  • Gastritis / metabolism
  • Gastritis / microbiology
  • Gastritis / prevention & control
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Leukotriene B4 / metabolism
  • Ligation
  • Male
  • Malondialdehyde / metabolism
  • Mice, Inbred ICR
  • Omeprazole / pharmacology
  • Oxidative Stress
  • Probiotics*
  • Proton Pump Inhibitors / pharmacology
  • Pylorus / surgery
  • Restraint, Physical
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / microbiology
  • Stomach Ulcer / pathology
  • Stomach Ulcer / prevention & control*
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • IL1B protein, mouse
  • Inflammation Mediators
  • Interleukin-1beta
  • Proton Pump Inhibitors
  • Tumor Necrosis Factor-alpha
  • Leukotriene B4
  • Ethanol
  • Malondialdehyde
  • 6-Ketoprostaglandin F1 alpha
  • Catalase
  • Superoxide Dismutase
  • Omeprazole