Abstract
The purpose of the study was to determine the inhibitory effects of Lactobacillus fermentum Suo (LF-Suo) on HCl/ethanol induced gastric injury in ICR (Institute for Cancer Research) mice and explain the mechanism of these effects through the molecular biology activities of LF-Suo. The studied mice were divided into four groups: healthy, injured, LF-Suo-L and LF-Suo-H group. After the LF-Suo intragastric administration, the gastric injury area was reduced compared to the injured group. The serum MOT (motilin), SP (substance P), ET (endothelin) levels of LF-Suo treated mice were lower, and SS (somatostatin), VIP (vasoactive intestinal peptide) levels were higher than the injured group mice. The cytokine IL-6 (interleukin 6), IL-12 (interleukin 12), TNF-α (tumor necrosis factor-α) and IFN-γ (interferon-γ) serum levels were decreased after the LF-Suo treatment. The gastric tissues SOD (superoxide dismutase), GSH-Px (glutathione peroxidase), NO (nitric oxide) and activities of LF-Suo treated mice were increased and MDA (malondialdehyde) activity was decreased compared to the injured group mice. By the RT-PCR assay, LF-Suo raised the occludin, EGF (epidermal growth factor), EGFR (epidermal growth factor receptor), VEGF (vascular endothelial growth factor), Fit-1 (fms-like tyrosine kinase-1), IκB-α (inhibitor kappaB-α), nNOS (neuronal nitric oxide synthase), eNOS (endothelial nitric oxide synthase), Mn-SOD, Cu/Zn-SOD, CAT (catalase) mRNA or protein expressions and reduced the COX-2, NF-κB (nuclear factor kappaB), and iNOS (inducible nitric oxide synthase) expressions in gastric tissues compared to the gastric injured group mice. A high concentration (1.0 × 109 CFU/kg b.w.) of LF-Suo treatment showed stronger anti-gastric injury effects compared to a low concentration of (0.5 × 109 CFU/kg b.w.) of LF-Suo treatment. LF-Suo also showed strong survival in pH 3.0 man-made gastric juice and hydrophobic properties. These results indicate that LF-Suo has potential use as probiotics for its gastric injury treatment effects.
Highlights
Ethanol is the main ingredient used in Chinese spirits and alcoholic beverages and because of its fat-soluble nature, it causes stomach injury, so alcohol abuse can cause acute erosive hemorrhagic gastritis and long-term drinking could cause stomach disorders and chronic atrophic gastritis [1].At high concentration of ethanol might cause stomach injury through direct erosion, and through metabolism ethanol converts to acetaldehyde, whose toxic effect may lead to stomach cancer [2].Different studies explain alcoholic gastric damage mechanism; showing that oxygen free radicals and lipid peroxidation chain reaction is one of the important mechanisms in stomach injury
The aim of the study was to determined the inhibitory effects of Lactobacillus fermentum Suo (LF-Suo) on gastric injury in vivo by observing mice stomach injury morphology, tissue damage and oxidation-related serum index, as well as changes of inflammatory cytokines in serum and the expression of oxidation and inflammation-related mRNA in stomach tissue
The SOD, GSH-Px, NO activities in gastric tissues of LF-Suo treated mice were increased and MDA activity was decreased compared to the injured group mice
Summary
Ethanol is the main ingredient used in Chinese spirits and alcoholic beverages and because of its fat-soluble nature, it causes stomach injury, so alcohol abuse can cause acute erosive hemorrhagic gastritis and long-term drinking could cause stomach disorders and chronic atrophic gastritis [1].At high concentration of ethanol might cause stomach injury through direct erosion, and through metabolism ethanol converts to acetaldehyde, whose toxic effect may lead to stomach cancer [2].Different studies explain alcoholic gastric damage mechanism; showing that oxygen free radicals and lipid peroxidation chain reaction is one of the important mechanisms in stomach injury. Ethanol is the main ingredient used in Chinese spirits and alcoholic beverages and because of its fat-soluble nature, it causes stomach injury, so alcohol abuse can cause acute erosive hemorrhagic gastritis and long-term drinking could cause stomach disorders and chronic atrophic gastritis [1]. At high concentration of ethanol might cause stomach injury through direct erosion, and through metabolism ethanol converts to acetaldehyde, whose toxic effect may lead to stomach cancer [2]. Different studies explain alcoholic gastric damage mechanism; showing that oxygen free radicals and lipid peroxidation chain reaction is one of the important mechanisms in stomach injury. During ethanol metabolic processes in the body, neutrophils release oxygen free radicals, causing endothelial damage, microcirculation disturbance and inhibits gastric injury healing. HCl could cause damage of gastric mucosa, and ethanol could reach the mucosa and induce cell rupture in the wall of blood vessels [4]
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