Bile-pancreatic duct ligation in rats excludes bile-pancreatic juice from the gut and induces acute pancreatitis. Bile-pancreatic juice exclusion from the gut results in increased plasma cholecystokinin (CCK) levels. CCK-A receptor-mediated exocrine pancreatic hyperstimulation is implicated in disease pathogenesis. In the present study, we show for the first time a progressive rise in CCK-A receptor protein expression in ligation-induced acute pancreatitis in rats. As CCK-A receptor induction could amplify CCK-mediated acinar hyperstimulation and exacerbate acinar cell stress with activation of the p38MAPK stress kinase pathway, we studied CCK-A receptor protein expression and p38MAPK activation in duct ligation-induced acute pancreatitis in rats. Compared to sham-operated controls, acute pancreatitis induced by bile-pancreatic duct ligation associates with a temporal increase in pancreatic CCK-A receptor protein expression, p38MAPK expression and activation, and NF-ĸB activation. These findings may have significance in the mechanism of disease pathogenesis in this experimental model.

Keywords:
Acute pancreatitis, Cholecystokinin, Cholecystokinin-A receptor, p38 MAP kinase, Stress-activated protein kinase, NF-ĸB, Signal transduction, Acinar cell, Donor rat model
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© 2004 S. Karger AG, Basel and IAP
2004
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