Beneficial effects of the commercial lactic acid bacteria product, Vigiis 101, on gastric mucosa and intestinal bacterial flora in rats

Li Kao, Te-Hua Liu, Tsung-Yu Tsai, Tzu-Ming Pan, Li Kao, Te-Hua Liu, Tsung-Yu Tsai, Tzu-Ming Pan

Abstract

Background: Gastric mucosal integrity is maintained through achieving a balance between potentially detrimental and protective factors. This study aimed to evaluate the effects of Vigiis 101 powder, a product consisting of dried Lactobacillus paracasei subsp. paracasei NTU 101 bacteria, on intestinal bacterial flora and acute damage to the gastric mucosa induced by pylorus ligation.

Method: Acute gastric injury were induced by pylorus ligation. Rats were orally treated with the vehicle or 0.15, 0.30, 1.50 g/kg (0.5-, 1-, and 5-x) Vigiis 101 for 8 weeks. We analyzed the intestinal microflora, short-chain fatty acids, antioxidant enzyme levels and gastric lesion.

Results: Daily treatment of rats with Vigiis 101 increased the levels of beneficial Bifidobacterium spp. and Lactobacillus spp., and reduced those of detrimental Clostridium perfringens and Enterobacteriaceae. Vigiis 101 treatment also markedly reduced gastric lesion areas by between 1.7 and 11.4%, and significantly increased the levels of the short-chain fatty acids (SCFAs): acetic acid, propionic acid, and butyric acid in cecal samples by 45-86%, 127-158%, and 20-211%, respectively, compared to non-treated controls. In the gastric mucosa of rats treated with Vigiis 101, the activity of superoxide dismutase and levels of prostaglandin E2 (PGE2) were enhanced, and the activity of lipid peroxidase reduced, relative to controls.

Conclusion: The up-regulation of PGE2 and SCFAs in the gastric mucosa is likely to stimulate mucus secretion and increase transmucosal resistance, thereby contributing to Vigiis 101-mediated protection from gastric mucosal lesions induced by pylorus ligation.

Keywords: Antioxidant; Gastric mucosa lesion; Lactobacillus paracasei subsp. paracasei NTU 101; Short-chain fatty acid.

Copyright © 2018. Published by Elsevier B.V.

Source: PubMed

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