Lactobacillus Reuteri DSM 17938 Protects Against Gastric Damage Induced by Ethanol Administration in Mice: Role of TRPV1/Substance P Axis

Nutrients. 2019 Jan 21;11(1):208. doi: 10.3390/nu11010208.

Abstract

This study aimed to evaluate the effect of Lactobacillus reuteri DSM 17938 (DSM) on ethanol-induced gastric injury, and if its possible mechanism of action is related to inhibiting the transient receptor potential vanilloid type 1 (TRPV1). We evaluated the effect of supplementing 10⁸ CFU•g body wt-1•day-1 of DSM on ethanol-induced gastric injury. DSM significantly reduced the ulcer area (1.940 ± 1.121 mm²) with 3 days of pretreatment. The effects of DSM supplementation were reversed by Resiniferatoxin (RTX), TRPV1 agonist (3 nmol/kg p.o.). Substance P (SP) (1 μmol/L per 20 g) plus 50% ethanol resulted in hemorrhagic lesions, and DSM supplementation did not reverse the lesion area induced by administering SP. TRPV1 staining intensity was lower, SP, malondialdehyde (MDA) and nitrite levels were reduced, and restored normal levels of antioxidant parameters (glutathione and superoxide dismutase) in the gastric mucosa in mice treated with DSM. In conclusion, DSM exhibited gastroprotective activity through decreased expression of TRPV1 receptor and decreasing SP levels, with a consequent reduction of oxidative stress.

Keywords: TRPV; alcohol; gastritis; neurokinin; probiotic.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Diterpenes / pharmacology
  • Ethanol / adverse effects*
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / microbiology
  • Gastric Mucosa / pathology*
  • Gastritis / chemically induced
  • Gastritis / metabolism
  • Gastritis / prevention & control
  • Glutathione / metabolism
  • Lactobacillus reuteri / classification
  • Lactobacillus reuteri / growth & development*
  • Malondialdehyde / metabolism
  • Mice
  • Probiotics / therapeutic use*
  • Protective Agents / therapeutic use
  • Species Specificity
  • Stomach / microbiology
  • Stomach / pathology
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / pathology
  • Stomach Ulcer / prevention & control*
  • Substance P / antagonists & inhibitors*
  • Superoxide Dismutase / metabolism
  • TRPV Cation Channels / antagonists & inhibitors*
  • TRPV Cation Channels / pharmacology

Substances

  • Antioxidants
  • Diterpenes
  • Protective Agents
  • TRPV Cation Channels
  • TRPV1 protein, mouse
  • TRPV1 receptor
  • Substance P
  • Ethanol
  • Malondialdehyde
  • resiniferatoxin
  • Superoxide Dismutase
  • Glutathione