Abstract
Background and Aims: In earlier experiments we have shown that exogenous application of prostaglandin E2 inhibits secretagogue stimulated enzyme secretion in isolated rat pancreatic acini. Also specific receptors for prostaglandin E2 were characterized on acinar cell membrane (Am. J. Physiol. 1991, 260, G711-19). Prostaglandins as mediators of inflammation are synthesized by the key enzyme cyclooxygenase (Cox or prostaglandin H synthase), of which two isoforms have been identified, Cox-1 and Cox-2. We are interested in two aspects of regulation of cell function through prostaglandins: Modulation of prostaglandin synthesis dependent on diet and through induction of pancreatitis in an animal model. Since a number of prostaglandins might be involved in these processes it appears reasonable to look at the regulation of the two cyclooxygenase isoforms by which all prostaglandins have to be synthesized. Methods and Results: We have developed an RT-PCR method to determine changes in the expression of Cox-1 and Cox-2 isoforms. Pancreatitis was induced in rats by different concentrations of cerulein. An optimal concentration for the induction of pancreatitis was determined. Pancreatic acini were isolated employing a collagenase digestion method. Total RNA was isolated from these acini from cerulein treated and untreated rats. We could detect both, Coxl and Cox-2, mRNA in isolated rat pancreatic acini. Amounts of Cox mRNA were standardized by comparison with GAPDH and actin expression. We also looked at and could exclude leukocyte infiltration in these tissue preparations. We will present data an induction and repression of cyclooxygenase transcription dependent on induced pancreatitis. We will discuss the correlation of enzyme expression, synthesis of prostaglandins and a potential cytoprotective role of prostaglandins. Conclusion: Cox-1 and Cox-2 are expressed in acinus cells of the pancreas with pancreatitis and in normal acini. These enzymes synthesize prostaglandins which may play a roll in mediation of pancreatitis.
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