Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, causes chronic abdominal pain, vomiting, diarrhea, weight loss and rarely death. Numerous treatments for IBD target the transcription factor NF-kappaB. This factor controls many genes involved in inflammation including those of cytokines and chemokines. These researchers looked at whether curcumin was able to affect the degree of inflammation of the colon (colitis) in mice treated with dinitrobenzene sulfonic acid (DNB). DNB was used to produce a predictable colitis in these mice. Curcumin was given by mouth 5 days before the DNB treatment. It reduced the amount of visually apparent damage in the colon. It also reduced NF-kappaB activation and the activity of the enzyme myeloperoxidase. Myeloperoxidase is a known marker for the accumulation of inflammatory cell infiltration in mouse models of colitis. They also measured the message for IL-1beta. This is one of the cytokines most important in IBD. The amount of this message, usually induced by DNB, was decreased in the curcumin treated mice. DNB reproducibly activated p38 mitogen-activated protein kinase measured in intestine cells of these mice. This level of activation was reduced by curcumin. They look under the microscope to see where this kinase activation was most reduced. They found that it was most reduced in cell of the intestinal mucosa. They concluded that curcumin is able to prevent the severity of this experimental colitis. They suggest that curcumin may be of value in treating human inflammatory bowel disease.
Curcumin attenuates DNB-induced murine colitis. [Am J Physiol Gastrointest Liver Physiol. 2003]