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This Article Full Text Full Text (PDF) All Versions of this Article: 294/4/G1094    most recent 00534.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Rifai, Y. Articles by Saccone, G. T. P. PubMed PubMed Citation Articles by Rifai, Y. Articles by Saccone, G. T. P.

NEUROREGULATION AND MOTILITY

The tripeptide analog feG ameliorates severity of acute pancreatitis in a caerulein mouse model

Departments of ¹Surgery, Centre for Neuroscience, ²Anatomy and Histology, and ³Anatomical Pathology, Flinders University, Flinders Medical Centre, Bedford Park, South Australia, Australia; and ⁴Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada

Submitted 16 November 2007 ; accepted in final form 21 February 2008

Acute pancreatitis (AP) is associated with significant morbidity and mortality; however, there is no specific treatment for this disease. A novel salivary tripeptide analog, feG, reduces inflammation in several different animal models of inflammation. The aims of this study were to determine whether feG reduced the severity of AP and modifies the expression of pancreatic ICAM-1 mRNA during AP in a mouse model. AP was induced in mice by hourly (x12) intraperitoneal injections of caerulein. A single dose of feG (100 µg/kg) was coadministered with caerulein either at time 0 h (prophylactic) or 3 h after AP induction (therapeutic). Plasma amylase and pancreatic MPO activities and pancreatic ICAM-1 mRNA expression (by RT-PCR) were measured. Pancreatic sections were histologically assessed for abnormal acinar cells and interstitial space. AP induction produced a sevenfold increase in plasma amylase, a tenfold increase in pancreatic MPO activity, and a threefold increase in interstitial space, and 90% of the acinar cells were abnormal. Prophylactic treatment with feG reduced the AP-induced plasma amylase activity by 45%, pancreatic MPO by 80%, the proportion of abnormal acinar cells by 30%, and interstitial space by 40%. Therapeutic treatment with feG significantly reduced the AP-induced abnormal acinar cells by 10% and the interstitial space by 20%. Pancreatic ICAM-1 mRNA expression was upregulated in AP and was reduced by 50% with prophylactic and therapeutic treatment with feG. We conclude that feG ameliorates experimental AP acting at least in part by modulating ICAM-1 expression in the pancreas.

salivary gland peptides; inflammation; neutrophils; ICAM-1; pancreas