Linked Life Data

15197232

Source:http://linkedlifedata.com/resource/pubmed/id/15197232

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-8-26
pubmed:abstractText
Oxidant stress has been implicated in the pathogenesis of inflammatory bowel disease. Antioxidant enzymes, such as superoxide dismutase (SOD), are candidate drugs for modulating this pathogenic factor. This study was designed to determine the therapeutic value of SOD in an experimental model of colitis and to study the mechanisms underlying its effects on intestinal inflammation. For that purpose, colitic (trinitrobenzene sulfonic acid-induced) and control rats were studied. Groups of colitic animals were treated with different doses of SOD (1, 4, or 13 mg/kg/day) or vehicle, starting after induction of colitis and during 7 days. Clinical and pathological markers of colitis severity and lipid peroxidation in colonic tissue were measured. Leukocyte-endothelial cell interactions in colonic venules and expression of vascular cell adhesion molecule 1 (VCAM-1) were determined. Development of colitis was associated with a significant loss in body weight, an increase in macroscopic and microscopic damage scores, and colonic myeloperoxidase activity. Administration of SOD significantly attenuated these changes in a dose-dependent manner and reduced lipid peroxidation in colonic tissue. The increase in leukocyte rolling and adhesion in colonic venules of colitic rats were significantly reduced by administration of SOD, 13 mg/kg/day. Development of colitis was associated with a marked increase in endothelial VCAM-1 expression, which was significantly reduced by treatment with SOD. In conclusion, treatment with SOD significantly reduces peroxidation reactions in the inflamed colon and affords significant amelioration of colonic inflammatory changes in experimental colitis. This effect is related to a reduction in VCAM-1 expression and leukocyte recruitment into the inflamed intestine.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
537-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15197232-Animals, pubmed-meshheading:15197232-Body Weight, pubmed-meshheading:15197232-Cell Adhesion, pubmed-meshheading:15197232-Cell Adhesion Molecules, pubmed-meshheading:15197232-Chemotaxis, Leukocyte, pubmed-meshheading:15197232-Colitis, pubmed-meshheading:15197232-Colon, pubmed-meshheading:15197232-Disease Models, Animal, pubmed-meshheading:15197232-Dose-Response Relationship, Drug, pubmed-meshheading:15197232-Down-Regulation, pubmed-meshheading:15197232-Intestinal Mucosa, pubmed-meshheading:15197232-Lipid Peroxidation, pubmed-meshheading:15197232-Male, pubmed-meshheading:15197232-Oxidative Stress, pubmed-meshheading:15197232-Peroxidase, pubmed-meshheading:15197232-Rats, pubmed-meshheading:15197232-Rats, Sprague-Dawley, pubmed-meshheading:15197232-Superoxide Dismutase, pubmed-meshheading:15197232-Trinitrobenzenesulfonic Acid, pubmed-meshheading:15197232-Vascular Cell Adhesion Molecule-1, pubmed-meshheading:15197232-Venules
pubmed:year
2004
pubmed:articleTitle
Superoxide dismutase ameliorates TNBS-induced colitis by reducing oxidative stress, adhesion molecule expression, and leukocyte recruitment into the inflamed intestine.
pubmed:affiliation
Department of Gastroenterology, Hospital Clínic, IDIBAPS, Villarroel 170, 08036 Barcelona, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't