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This dissertation, A Study on the Role of Probiotic Lactobacillus Rhamnosus GG on Gastric Mucosal Damages in Rats by Kai-yee, Lam, 林佳儀, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract Abstract of the thesis entitled A study on the role of probiotic Lactobacillus rhamnosus GG on gastric mucosal damages in rats Submitted by Lam Kai-Yee For the degree of Master of Philosophy at the University of Hong Kong In August 2006 The gastrointestinal (GI) tract is colonized by a vast community of microorganisms and maintenance of the microbial balance is essential for gut health. For decades, probiotics have been shown to maintain the GI equilibrium of indigenous microflora. Although numerous studies have advocated their use for the prevention and treatment of various GI disorders, the role of probiotics in gastric mucosal damage has been comparatively neglected. The aim of this study is to investigate the beneficial effects of a probiotic strain Lactobacillus rhamnosus GG (LGG) on acetic acid-induced gastric ulcer and ethanol-induced gastric lesions and to elucidate the mechanisms involved. The study found that LGG significantly and dose-dependently reduced gastric ulcer area. The cell apoptosis to cell proliferation ratio was strongly decreased and accompanied by significant upregulation of ornithine decarboxylase (ODC) and B-cell lymphoma 2 (Bcl-2) protein expressions at the ulcer margin. Angiogenesis was also significantly stimulated together with the induction of vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) expression. Furthermore, LGG up-regulated the phosphorylation levels of epidermal growth factor receptor (EGFR) and the downstream extracelluar signal-regulated kinase 1/2 (Erk1/2) iwithout altering total EGFR and Erk1/2 expression. These findings suggest that LGG enhanced gastric ulcer healing via the attenuation of cell apoptosis to cell proliferation ratio and increase in angiogenesis. Regulators of these processes such as ODC, Bcl-2, VEGF, COX-2, EGFR and Erk1/2 are likely to be involved in the ulcer healing action of LGG. LGG pretreatment also significantly reduced ethanol-induced gastric lesions in a dose-dependent manner. This was accompanied by the increase of basal mucosal prostaglandin E (PGE ) level and endothelial nitric oxide synthase (eNOS) protein 2 2 expression. In addition, LGG attenuated the suppressive action of ethanol on mucus layer, mucin 6 (muc6) mRNA expression and transmucosal resistance, and reversed the stimulatory action of ethanol on cellular apoptosis in the gastric mucosa. It is suggested that the protective role of LGG on ethanol-induced gastric mucosal lesions is likely attributable to the upregulation of PGE and eNOS, which in turn, stimulates the mucus secretion to increase the transmucosal resistance and subsequently protects cells from apoptosis in the gastric mucosa. The study's findings indicate the capability of LGG to act as a therapeutic and prophylactic agent in treating and preventing gastric damage. ii DOI: 10.5353/th_b3734005 Subjects: LactobacillusGastrointestinal diseases - Animal models

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