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      Inhibition of ulcerative colitis in mice after oral administration of a polyphenol-enriched cocoa extract is mediated by the inhibition of STAT1 and STAT3 phosphorylation in colon cells.

      Journal of Agricultural and Food Chemistry
      Animals, Cacao, chemistry, Cell Line, Colitis, Ulcerative, drug therapy, genetics, metabolism, Disease Models, Animal, Down-Regulation, drug effects, Female, Flavonoids, administration & dosage, Humans, Mice, Mice, Inbred BALB C, Phenols, Phosphorylation, Plant Extracts, Polyphenols, STAT1 Transcription Factor, STAT3 Transcription Factor

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          Abstract

          We studied a polyphenol-enriched cocoa extract (PCE) with epicatechin, procyanidin B2, catechin, and procyanidin B1 as the major phenolics for its anti-inflammatory properties against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. PCE reduced colon damage, with significant reductions in both the extent and the severity of the inflammation as well as in crypt damage and leukocyte infiltration in the mucosa. Analysis ex vivo showed clear decreases in the production of nitric oxide, cyclooxygenase-2, pSTAT-3, and pSTAT1α, with NF-κB p65 production being slightly reduced. Moreover, NF-κB activation was reduced in RAW 264.7 cells in vitro. In conclusion, the inhibitory effect of PCE on acute UC induced by DSS in mice was attenuated by oral administration of PCE obtained from cocoa. This effect is principally due to the inhibition of transcription factors STAT1 and STAT3 in intestinal cells, with NF-κB inhibition also being implicated.

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