The effect of octreotide on pancreatic damage in TNBS-induced colitis

Surg Innov. 2006 Jun;13(2):102-8. doi: 10.1177/1553350606291337.

Abstract

Inflammatory bowel disease, a chronic condition of the intestine, is associated with numerous extraintestinal manifestations, including pancreatitis. This study investigated the effect of octreotide administration on oxidative damage in a rat model of colitis induced by 2,4,6-trini-trobenzene sulfonic (TNBS) acid. Colonic and pancreatic malondialdehyde and glutathione levels are indicators of oxidative damage, and TNBS-induced colitis significantly increased the colonic and pancreatic malondialdehyde levels and decreased glutathione levels. Octreotide treatment was associated with decreased malondialdehyde levels and increased glutathione levels in the colonic and pancreatic tissue. The colonic mucosal structure was preserved and pancreatic inflammation decreased in rats treated with octreotide. Octreotide also significantly decreased nuclear factor-kB expression by immunohisto-chemistry in the colonic and pancreatic tissue compared with TNBS-induced colitis group. Octreotide appears to have protective effects against TNBS-induced colonic and pancreatic damage. These results imply the reduction in mucosal damage owing to the anti-inflammatory and antioxidant effects of octreotide.

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colitis / metabolism*
  • Gastrointestinal Agents / therapeutic use*
  • Glutathione / metabolism
  • Male
  • Malondialdehyde / metabolism
  • NF-kappa B / metabolism
  • Octreotide / therapeutic use*
  • Oxidative Stress / physiology
  • Pancreatitis / drug therapy*
  • Pancreatitis / etiology
  • Pancreatitis / metabolism*
  • Rats
  • Rats, Wistar
  • Trinitrobenzenesulfonic Acid

Substances

  • Gastrointestinal Agents
  • NF-kappa B
  • Malondialdehyde
  • Trinitrobenzenesulfonic Acid
  • Glutathione
  • Octreotide