S N Porter1, G S Howarth, R N Butler. 1. Dept. of Physiology, The University of Adelaide, and South Australia Cooperative Research Centre for Tissue Growth and Repair, Australia.
Abstract
BACKGROUND: Lipid peroxidation is a potential mechanism of bowel damage in colitis. The effect of oral consumption of a bovine whey-derived growth factor extract (WGFE) on lipid peroxidation was assessed using the ethane breath test in the dextran sulphate sodium (DSS) model of ulcerative colitis (UC) in rats. METHODS: Groups of rats consumed water (control), 2% DSS in drinking water, 2% DSS with a WGFE-supplemented diet, or 2% DSS plus prednisolone (1 mg x kg(-1) x day(-1)) for 6 weeks, changing to sulphasalazine (100 mg x kg(-1) x day(-1)) for the subsequent 4 weeks. Ethane breath tests were conducted on all animals on days 2, 4, 6, 8, and 10 (acute phase) and weeks 3, 6, and 9 (chronic phase) after commencement of DSS consumption. RESULTS: There were no significant differences in ethane production between any groups during the acute phase. Ethane was significantly increased (P < 0.05) in rats consuming DSS alone in week 6 compared with control but had decreased to control levels by week 9. WGFE and conventional therapy were effective in suppressing ethane production in week 3. CONCLUSIONS: WGFE is as effective as conventional therapies at limiting ethane production and thus ostensibly colonic lipid peroxidation in the early phases of experimental chronic UC.
BACKGROUND:Lipid peroxidation is a potential mechanism of bowel damage in colitis. The effect of oral consumption of a bovine whey-derived growth factor extract (WGFE) on lipid peroxidation was assessed using the ethane breath test in the dextran sulphate sodium (DSS) model of ulcerative colitis (UC) in rats. METHODS: Groups of rats consumed water (control), 2% DSS in drinking water, 2% DSS with a WGFE-supplemented diet, or 2% DSS plus prednisolone (1 mg x kg(-1) x day(-1)) for 6 weeks, changing to sulphasalazine (100 mg x kg(-1) x day(-1)) for the subsequent 4 weeks. Ethane breath tests were conducted on all animals on days 2, 4, 6, 8, and 10 (acute phase) and weeks 3, 6, and 9 (chronic phase) after commencement of DSS consumption. RESULTS: There were no significant differences in ethane production between any groups during the acute phase. Ethane was significantly increased (P < 0.05) in rats consuming DSS alone in week 6 compared with control but had decreased to control levels by week 9. WGFE and conventional therapy were effective in suppressing ethane production in week 3. CONCLUSIONS: WGFE is as effective as conventional therapies at limiting ethane production and thus ostensibly colonic lipid peroxidation in the early phases of experimental chronic UC.