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dc.contributor.advisorHowarth, Gordon Stanleyen
dc.contributor.advisorTran, Cuong Duyen
dc.contributor.authorAbimosleh, Suzanne Mashtouben
dc.description.abstractSeveral disorders of the gastrointestinal (GI) tract including ulcerative colitis, chemotherapy-induced mucositis and non-steroidal anti-inflammatory drug (NSAID)- induced enteropathy, are characterised by inflammation, ulceration, mucosal damage and malabsorption. Treatment options are variably effective, highlighting the need to broaden therapeutic approaches, including adjunctive strategies. Emu Oil, derived from subcutaneous and retroperitoneal Emu adipose tissue, is a rich source of fatty acids (FA). Despite limited rigorous scientific studies, topically applied Emu Oil has demonstrated potent anti-inflammatory properties in vivo. Previously, orally administered Emu Oil improved intestinal architecture in a rat model of mucositis, with early indications of enhanced intestinal repair. Accordingly, this thesis investigated the effects of orally administered Emu Oil in rat models of colitis (colonic damage), NSAID-enteropathy (small intestinal [SI] damage) and on the time course of SI repair in chemotherapy-induced mucositis. In the current study, Emu Oil improved colonic tissue damage associated with dextran sulphate sodium-induced colitis in Sprague Dawley rats and facilitated the repair process (Chapter 2). Improvements were indicated histologically by reduced intestinal damage severity scores and enhanced crypt compensatory elongation in the colon. These findings suggested the potential for Emu Oil to augment conventional treatment approaches for colitis. The effectiveness of Emu Oil in the colon provided impetus to further investigate Emu Oil action proximally, in the SI. In a rat model of chemotherapy (5-Fluorouracil; 5- FU)-induced mucositis, Emu Oil maintained SI villus height and crypt depth during the phase of maximal damage (Chapter 3). This was followed by an enhanced compensatory mucosal thickening, suggesting an acceleration of the repair process. Furthermore, Emu Oil significantly decreased myeloperoxidase (MPO) activity, indicative of acute inflammation, in the jejunum and ileum of 5-FU-injected rats. Potent anti-inflammatory properties of Emu Oil were reaffirmed in NSAID (Indomethacin)-induced enteropathy, whereby MPO activity in the jejunum and ileum of Indomethacin-treated rats was markedly decreased following Emu Oil administration (Chapter 4). Treatments for diseases such as coronary artery disease and GI disorders seek to minimise oxidative damage by free radicals through the use of antioxidants. Oils derived from ratites (flightless birds) predominantly comprise FA varying in composition between ratite species. The influence of farm location, rendering method, duration and storage mode was investigated for free radical scavenging activity (RSA) against 2,2-diphenyl-1-picryl hydracyl and primary oxidation status of Ratite Oils (Chapter 5). Emu Oil conferred the greatest RSA compared to Ostrich and Rhea Oil, potentially attributed to its high unsaturated FA: saturated FA ratio and non-triglyceride fraction minor constituents. Rendering and storage variables impacted on Emu Oil RSA and primary oxidation. This thesis identified Emu Oil as a safe, renewable and economical means to augment pharmaceutical options for GI disorders. A new mechanism of action for Emu Oil could represent a promotion of repair from injury together with decreased SI inflammation. This suggests potential for Emu Oil as an adjunct to conventional treatment approaches for colitis, cancer management and long-term NSAID usage.en
dc.subjectemu oil; ulcerative colitis; chemotherapy-induced mucositis; NSAID-induced enteropathy; inflammation; intestinal; rat models; repairen
dc.titleEmu oil promotes intestinal repair in rat models of enteric inflammation.en
dc.contributor.schoolSchool of Medical Sciencesen
dc.provenanceThis electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at:
dc.provenanceCopyright material removed from digital thesis. See print copy in University of Adelaide Library for full text.en
dc.description.dissertationThesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2013en
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