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Hepatocyte growth factor and omega-3–enriched feeds have a synergistic effect on mucosal mass in an animal model of inflammatory bowel disease

Abstract Background Hepatocyte growth factor (HGF) decreases intestinal inflammation and cytokine levels in an animal model of inflammatory bowel disease (IBD). Luminal omega-3 (OM-3) is anti-angiogenic, reduces inflammation, and may decrease symptoms in patients with Crohn's disease. This stud...

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Published in:Journal of pediatric surgery 2012, Vol.47 (1), p.194-198
Main Authors: Katz, Michael S, Thatch, Keith A, Schwartz, Marshall Z
Format: Article
Language:English
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Summary:Abstract Background Hepatocyte growth factor (HGF) decreases intestinal inflammation and cytokine levels in an animal model of inflammatory bowel disease (IBD). Luminal omega-3 (OM-3) is anti-angiogenic, reduces inflammation, and may decrease symptoms in patients with Crohn's disease. This study evaluates the synergism of HGF and OM-3. Methods Twenty adult female transgenic HLA-B27 rats were divided into 4 groups: group 1: regular feeds, IV saline; group 2: OM-3–enriched feeds, IV saline; group 3: regular feeds, IV HGF (150 µg/kg per day); and group 4: OM-3–enriched feeds, IV HGF(150 µg/kg per day). Rats were killed at 14 days after pump placement. Small and large bowel mucosa was harvested, and DNA and protein were extracted and quantified. Statistical analysis was done by analysis of variance with post-hoc Tukey's HSD test. Results Content of protein and DNA in the ileum were significantly increased by supplementation of HGF ( P < .001, P < .01, respectively) alone. OM-3 significantly increased protein content but not DNA ( P = .02, P = 0.3, respectively). Combined, they had a synergistic effect greater than either supplement alone ( P = .0001, P = .002, respectively). In the colon, HGF and OM-3 did not significantly increase protein or DNA content individually or together. Conclusions This is the first demonstration of the synergistic effect of a growth factor (HGF) and a dietary supplement (OM-3) in an immunologic model of IBD.
ISSN:0022-3468
1531-5037
DOI:10.1016/j.jpedsurg.2011.10.043