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1 Department of Pharmacology, National University of Singapore, Singapore, Singapore
2 Department of Pharmacology, ACRAF SpA, Rome, Italy
* To whom correspondence should be addressed. E-mail: mbhatia{at}nus.edu.sg.
Chemokines are believed to play a key role in the pathogenesis of acute pancreatitis.
We have earlier shown that pancreatic acinar cells produce the chemokine MCP-1 in
response to caerulein hyperstimulation, demonstrating that acinar-derived MCP-1 is
an early mediator of inflammation in acute pancreatitis. Blocking chemokine
production or action is a major target for pharmacological intervention in a variety of
inflammatory diseases, such as acute pancreatitis. Bindarit (2-methyl-2-[[1-
(phenylmethyl)-1H-indazol-3yl]methoxy]propanoic acid) has been shown to
preferentially inhibit MCP-1 production in vitro in monocytes and in vivo, without
affecting the production of the cytokines IL-1, IL-6, or the chemokines IL-8, MIP-1
and RANTES. The present study aimed to define the role of MCP-1 in acute
pancreatitis by the use of bindarit. In a model of acute pancreatitis induced by
caerulein hyperstimulation, prophylactic as well as therapeutic treatment with bindarit
significantly reduced MCP-1 levels in the pancreas. Also, this treatment significantly
protected mice against acute pancreatitis as evident by attenuated hyperamylasemia
neutrophil sequestration in the pancreas (pancreatic MPO activity), and pancreatic
acinar cell injury/necrosis on histological examination of pancreas sections.
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