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|Title:||Treatment with bindarit, a blocker of MCP-1 synthesis, protects mice against acute pancreatitis|
|Authors:||Bhatia, M. |
|Source:||Bhatia, M., Ramnath, R.D., Chevali, L., Guglielmotti, A. (2005-06). Treatment with bindarit, a blocker of MCP-1 synthesis, protects mice against acute pancreatitis. American Journal of Physiology - Gastrointestinal and Liver Physiology 288 (6 51-6) : G1259-G1265. ScholarBank@NUS Repository. https://doi.org/10.1152/ajpgi.00435.2004|
|Abstract:||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 monocyte chemotactic protein (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. 2-Methyl-2-[[1-(phenylmethyl)-1H-indazol- 3yl]methoxy] propanoic acid (bindarit) 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, protein macrophage inflammatory-1α, and RANTES. The present study aimed to define the role of MCP-1 in acute pancreatitis with 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. Copyright © 2005 the American Physiological Society.|
|Source Title:||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|Appears in Collections:||Staff Publications|
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