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The effect of restraint stress on the normal colon and on intestinal inflammation in a model of experimental colitis.

Abstract
Stress may induce development of inflammation in animal models of colitis. The effects of restraint stress on oxidative damage and on antioxidants in the normal colonic mucosa were studied. The effect of stress on the severity of indicators of inflammation, as well as the importance of mucosal substance P (SP) as a mediator of this effect were investigated in the TNBS-colitis model. Restraint stress significantly increased malondialdehyde levels and reduced levels of low-molecular-weight-antioxidants in the normal colon. ATP and the mucosal "energy charge" decreased substantially with chronic stress. Chronic stress worsened the extent of inflammation in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Mucosal SP content was not affected by exposure to chronic stress but increased after induction of colitis. The increase was greater when colitis was induced after exposure to stress. We conclude that chronic restraint stress causes oxidative damage to the normal colon and aggravates intestinal inflammation induced by TNBS. This effect may be mediated by SP.
AuthorsEran Israeli, Tiberiu Hershcovici, Eduard Berenshtein, Giulliana Zannineli, Dov Wengrower, Ofra Weiss, Mordechai Chevion, Eran Goldin
JournalDigestive diseases and sciences (Dig Dis Sci) Vol. 53 Issue 1 Pg. 88-94 (Jan 2008) ISSN: 0163-2116 [Print] United States
PMID17565472 (Publication Type: Journal Article)
Chemical References
  • Biomarkers
  • Substance P
  • Malondialdehyde
  • Trinitrobenzenesulfonic Acid
Topics
  • Animals
  • Biomarkers (metabolism)
  • Chromatography, High Pressure Liquid
  • Colitis (chemically induced, metabolism, pathology)
  • Colon (physiology)
  • Disease Models, Animal
  • Female
  • Intestinal Mucosa (metabolism, pathology)
  • Malondialdehyde (metabolism)
  • Oxidative Stress (physiology)
  • Radioimmunoassay
  • Rats
  • Restraint, Physical
  • Severity of Illness Index
  • Stress, Physiological
  • Substance P (metabolism)
  • Trinitrobenzenesulfonic Acid (toxicity)

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