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Journal Article
Research Support, Non-U.S. Gov't
Emu oil increases colonic crypt depth in a rat model of ulcerative colitis.
Digestive Diseases and Sciences 2012 April
BACKGROUND: Current treatments for the inflammatory bowel diseases, encompassing Crohn's disease and ulcerative colitis, are variably effective. Emu oil, extracted from emu fat, predominantly comprises fatty acids, with purported claims of anti-inflammatory properties.
AIM: We evaluated emu oil for its potential to ameliorate dextran sulphate sodium (DSS)-induced colitis in rats.
METHODS: Male Sprague-Dawley Rats were allocated to treatment groups (n = 8). Groups 1 and 2 consumed water and were gavaged (1 ml) daily with water (group 1) or emu oil (group 2) from days 0 to 10. Groups 3-6 ingested 2% DSS in the drinking water from days 5 to 10 and were gavaged from days 0 to 10 with water (group 3), 0.5 ml emu oil (group 4) or 1 ml emu oil (group 5). Group 6 received 1 ml emu oil after commencing DSS treatment (days 6-10). Disease activity index, metabolic parameters, (13)C-sucrose breath test, and histological colonic damage severity and crypt depth were assessed.
RESULTS: Emu oil in DSS-treated rats reduced colonic damage severity compared to DSS-controls (up to threefold; P < 0.001). In DSS-treated rats, crypts in the proximal colon were lengthened by 0.5 ml emu oil (373 ± 18 μm), compared with DSS-controls (302 ± 8 μm); whilst in the distal colon (DSS control: 271 ± 17 μm), crypt depth was greater following 0.5 ml emu oil (352 ± 22 μm) and 1 ml emu oil (341 ± 9 μm) and also when emu oil was administered post-DSS commencement (Group 6: 409 ± 16 μm; P < 0.05). Emu oil did not significantly affect other parameters of colonic architecture.
CONCLUSIONS: Emu oil improved tissue damage associated with colitis, suggesting its potential as a unique formulation to augment conventional treatment approaches for IBD.
AIM: We evaluated emu oil for its potential to ameliorate dextran sulphate sodium (DSS)-induced colitis in rats.
METHODS: Male Sprague-Dawley Rats were allocated to treatment groups (n = 8). Groups 1 and 2 consumed water and were gavaged (1 ml) daily with water (group 1) or emu oil (group 2) from days 0 to 10. Groups 3-6 ingested 2% DSS in the drinking water from days 5 to 10 and were gavaged from days 0 to 10 with water (group 3), 0.5 ml emu oil (group 4) or 1 ml emu oil (group 5). Group 6 received 1 ml emu oil after commencing DSS treatment (days 6-10). Disease activity index, metabolic parameters, (13)C-sucrose breath test, and histological colonic damage severity and crypt depth were assessed.
RESULTS: Emu oil in DSS-treated rats reduced colonic damage severity compared to DSS-controls (up to threefold; P < 0.001). In DSS-treated rats, crypts in the proximal colon were lengthened by 0.5 ml emu oil (373 ± 18 μm), compared with DSS-controls (302 ± 8 μm); whilst in the distal colon (DSS control: 271 ± 17 μm), crypt depth was greater following 0.5 ml emu oil (352 ± 22 μm) and 1 ml emu oil (341 ± 9 μm) and also when emu oil was administered post-DSS commencement (Group 6: 409 ± 16 μm; P < 0.05). Emu oil did not significantly affect other parameters of colonic architecture.
CONCLUSIONS: Emu oil improved tissue damage associated with colitis, suggesting its potential as a unique formulation to augment conventional treatment approaches for IBD.
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