Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-8-13
pubmed:abstractText
This study evaluated whether arginine (Arg) supplementation could attenuate gut injury induced by Escherichia coli lipopolysaccharide (LPS) challenge through an anti-inflammatory role in weaned pigs. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS+0.5 % Arg; (4) LPS+1.0 % Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h post-injection, pigs were killed for evaluation of small intestinal morphology and intestinal gene expression. Within 48 h of challenge, 0.5 % Arg alleviated the weight loss induced by LPS challenge (P = 0.025). In all three intestinal segments, 0.5 or 1.0 % Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P < 0.05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P < 0.01). The 0.5 % Arg prevented the elevation of jejunal IL-6 mRNA abundance (P = 0.082), and jejunal (P = 0.030) and ileal (P = 0.039) TNF-alpha mRNA abundance induced by LPS challenge. The 1.0 % Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P = 0.053) and jejunal TNF-alpha mRNA abundance (P = 0.003) induced by LPS challenge. The 0.5 % Arg increased PPARgamma mRNA abundance in all three intestinal segments (P < 0.10), and 1.0 % Arg increased duodenal PPARgamma mRNA abundance (P = 0.094). These results indicate that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal pro-inflammatory cytokines through activating PPARgamma expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1475-2662
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
552-60
pubmed:dateRevised
2009-5-20
pubmed:meshHeading
pubmed-meshheading:18275628-Animals, pubmed-meshheading:18275628-Anti-Inflammatory Agents, pubmed-meshheading:18275628-Arginine, pubmed-meshheading:18275628-Biological Markers, pubmed-meshheading:18275628-Dietary Supplements, pubmed-meshheading:18275628-Duodenum, pubmed-meshheading:18275628-Escherichia coli, pubmed-meshheading:18275628-Female, pubmed-meshheading:18275628-Ileum, pubmed-meshheading:18275628-Interleukin-6, pubmed-meshheading:18275628-Intestinal Mucosa, pubmed-meshheading:18275628-Intestine, Small, pubmed-meshheading:18275628-Jejunum, pubmed-meshheading:18275628-Lipopolysaccharides, pubmed-meshheading:18275628-Male, pubmed-meshheading:18275628-PPAR gamma, pubmed-meshheading:18275628-RNA, Messenger, pubmed-meshheading:18275628-Swine, pubmed-meshheading:18275628-Tumor Necrosis Factor-alpha, pubmed-meshheading:18275628-Weaning
pubmed:year
2008
pubmed:articleTitle
Dietary arginine supplementation alleviates intestinal mucosal disruption induced by Escherichia coli lipopolysaccharide in weaned pigs.
pubmed:affiliation
Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China. yulanflower@126.com
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't