Ameliorative Activities by Ellagic acid on Gut dysbiosis during starvation induced gastric ulceration in Rats: The role of Enterococcus feacium

Authors

  • A. Adekoya
  • U. Akpamu
  • F. Omeonu
  • T. Iyiola
  • A. Salami
  • F. Oluwole

Keywords:

Ellagic acid, starvation induced gastric ulcer, Enterococcus faecium, gut microflora metabolite

Abstract

Starvations result to formation of gastric ulcer, and microbiome dysbiosis. During starvation, there is increased release of iron stores, which can either be beneficial for growth of some gut flora or impedance to activities of some polyphenols. Polyphenols and gut microflora homeostasis are pivotal during healing of gastric ulcers. Ellagic acid (EA); a plant-derived poly-phenol, has proven to be gastro-protective, but there is dearth of information on its activities on commensal Enterococcus faecium during starvation induced gastric ulcer and hence the aim of this study. Thirty rats were grouped into 6 as control, untreated or treated with cimetidine (50mg/kg), 75mg/kg, 50mg/kg or 25mg/kg EA for 4 weeks. Gastric ulcer was induced by depriving the animals of food for the last 6 days in groups 2 to 6. Ulcer index was determined and gastric biochemicals were estimated from stomach homogenate, while microorganisms were assessed in gastric sample as well as tissue histological studies. The data were analysed using ANOVA with Turkey's posthoc significance test at p ≤ 0.05 significance.

Ellagic acid treatments significantly decreased mean ulcer index, lipid peroxidation, hydrogen peroxide levels and H+/K+-ATPase activity compared with starved-untreated. Gastric mucin, sulfhydryl, and catalase activities were significantly increased in low- and medium-EA treated groups compared with starved-untreated. Gastric carbonyl level significantly decreased only in low-EA group compared with starved-untreated. Nitric oxide levels significantly increased in medium- and high-EA treated groups. Gut derived commensal microflora Enterococcus faecium; and probiotic bacteria Lactobacillus fermentum, Lactobacillus delbrueckii and Pedicoccus acidilactici were up-regulated in all EA treatment groups.

In conclusion, EA attenuated starvation induced gastric ulceration via increased anti-oxidative mechanisms, nitric-oxide and reduced gastric H+/K+-ATPase activities, which enabled proliferation of gut-commensal microflora; Enterococcus faecium

Published

2025-01-29

Issue

Section

Nutrition/Natural Product and Drug Development