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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]

Curcumin, part of the spice turmeric, prevents cancers in rodent intestines. It is being studied in clinical trials of humans to prevent colon cancer. Very little of dietary curcumin goes into the blood stream. These researchers further evaluated the notion that curcumin is metabolized in the intestine. They compared its metabolism in parts intestinal cells with the same parts of liver cells from humans and rats. They also studied the metabolism of curcumin in rat intestinal sacs grown in test tubes. Curcumin conjugates and reduction products were identified using high-performance liquid chromatography. Curcumin glucuronide was found in microsomes of liver and intestine cells. Curcumin sulfate, tetrahydrocurcumin, and hexahydrocurcumin found as curcumin metabolites in the cytosol of these cells. Cytosol is fluid part of the cell. In cells from the intestine, curcumin was conjugated more in human cells than in rat cells. The opposite occurred in cells from the liver. The cytosol of human intestinal and liver cells reduced curcumin 18 and 5 fold more, respectively, than did the same type of cell from rats. The intact rat gut sacs produced curcumin sulfate from curcumin. They concluded that curcumin is metabolized greatly, both conjugated and reduced, in the in the gastrointestinal tract and metabolized more by human than by rat intestines. The metabolism of curcumin should be taken into consideration in planning trials of curcumin given by mouth.

Metabolism of the cancer chemopreventive agent cur…[Cancer Epidemiol Biomarkers Prev. 2002]

Mice were given a compound called dinitrobenzene sulfonic acid in order to give them colitis. Some of the mice were given 50mg/kg of curcumin, a component of the Indian spice turmeric, for 10 days prior to being given the chemical. The treated mice showed fewer intestinal lesions, and had a reduction in inflammatory markers that were linked to the curcumin. This preliminary research on mice suggests that turmeric may be helpful in treating IBD in humans.

Link to first study

Link to second study