Please use this identifier to cite or link to this item: https://doi.org/10.1152/ajpgi.00435.2004
Title: Treatment with bindarit, a blocker of MCP-1 synthesis, protects mice against acute pancreatitis
Authors: Bhatia, M. 
Ramnath, R.D. 
Chevali, L. 
Guglielmotti, A.
Keywords: Bindarit
Caerulein
Myeloperoxidase
Issue Date: Jun-2005
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
URI: http://scholarbank.nus.edu.sg/handle/10635/108050
ISSN: 01931857
DOI: 10.1152/ajpgi.00435.2004
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