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Am J Physiol Gastrointest Liver Physiol 285: G586-G592, 2003. First published April 30, 2003; doi:10.1152/ajpgi.00463.2002
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INFLAMMATION/IMMUNITY/MEDIATORS

Amelioration of TNBS-induced colon inflammation in rats by phospholipase A2 inhibitor

M. Krimsky,1 S. Yedgar,1 L. Aptekar,2 O. Schwob,1 G. Goshen,3 A. Gruzman,4 S. Sasson,4 and M. Ligumsky2

1Department of Biochemistry, Hadassah Medical School, 2Gastroenterology Unit, Hadassah University Hospital, 3Department of Oral Biology, School of Dental Medicine, and 4Department of Pharmacology, School of Pharmacy, Hebrew University Faculty of Medicine, Jerusalem, Israel 91120

Submitted 28 October 2002 ; accepted in final form 23 April 2003

The pathophysiology of inflammatory bowel disease (IBD) involves the production of diverse lipid mediators, namely eicosanoids, lysophospholipids, and platelet-activating factor, in which phospholipase A2 (PLA2) is the key enzyme. Accordingly, it has been postulated that control of lipid mediator production by inhibition of PLA2 would be useful for the treatment of IBD. This hypothesis was tested in the present study by examining the therapeutic effect of a novel extracellular PLA2 inhibitor (ExPLI), composed of carboxymethylcellulose-linked phosphatidylethanolamine (CMPE), on trinitrobenzenesulfonic acid-induced colitis. Intraperitoneal administration of CMPE suppressed the colitis as measured by mortality rate, intestinal permeability, plasma PLA2 activity, intestinal myeloperoxidase activity, and histological morphometry. Current therapeutic approaches for inflammatory conditions focus on the selective control of a lipid mediator(s) (e.g., prostaglandins or leukotrienes). The present study supports the concept that inclusive control of lipid mediator production by PLA2 inhibition is a plausible approach to the treatment of colitis and introduces the ExPLIs as a prototype of a novel NSAID for the treatment of intestinal inflammation.

inflammatory bowel disease; colitis; nonsteroidal anti-inflammatory drugs


Address for reprint requests and other correspondence: S. Yedgar Dept. of Biochemistry, Hebrew Univ.-Hadassah Medical School, Jerusalem, Israel 91120 (E-mail: yedgar{at}md2.huji.ac.il).




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