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Curcumin may be an inexpensive, well-tolerated, and effective therapy for inflammatory bowel disease

August 25, 2003 (Bethesda, MD) Inflammatory bowel disease (IBD) refers to Crohn's disease and ulcerative colitis, debilitating illnesses characterized by chronic recurrent ulceration of the bowel, abdominal pain, digestive problems, diarrhea or constipation. The National Institutes of Health estimates that some two million Americans suffer from this disorder, which is of unknown origin, but likely caused by a combination of genetic, environmental, and immunologic factors.

Medical researchers have made considerable efforts to establish a genetic linkage between Crohn's disease and the NOD2 protein associated with programmed cell death and activation of NF- B, a transcription factor involved in the production of cytokines and chemokines necessary for inflammation.

Regulation of NF- B function has been documented by several agents used in the management of IBD, such as corticosteroids, sulfasalazine, and 5-aminosalicylates (5-ASA). Furthermore, antisense oligonucleotides directed against the p65 subunit (a polypeptide contributing to the activation of NF- B) have been shown to diminish disease activity in an animal model of colitis. Recent work has shown that dietary constituents such as curcumin may also potently inhibit NF- B and diminish attenuate proinflammatory molecule expression. Curcumin is a component of the spice turmeric (Curcuma longa) used in curries and mustard, whose anti-inflammatory properties have been recognized for years. These effects are related, in part, to inhibition of the activities of the cyclooxygenase, lipoxygenase, and NF- B in several cell systems. Furthermore, its role in the attenuation of colonic cancer in animal models has also been established.

Management of IBD involves the use of 5-ASA and immunosuppressives such as corticosteroids and 6-mercaptopurine as well as its precursor azathioprine. Novel agents such as monoclonal antibodies against TNF- have been developed and demonstrate clinical efficacy. How
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
25-Aug-2003


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