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Oligonol Inhibits Dextran Sulfate Sodium-Induced Colitis and Colonic Adenoma Formation in Mice

Cited 28 time in Web of Science Cited 26 time in Scopus
Authors
Yum, Hye-Won; Zhong, Xiancai; Park, Jin; Na, Hye-Kyung; Kim, Nayoung; Lee, Hye Seung; Surh, Young-Joon
Issue Date
2013-07
Citation
Antioxidants and Redox Signaling, Vol.19 No.2, pp.102-114
Abstract
Aims: To evaluate the effects of oligonol administration on experimentally induced colitis and colonic adenoma formation. Results: Oral administration of oligonol protected against mouse colitis induced by dextran sulfate sodium (DSS). Under the same experimental conditions, oligonol administration significantly inhibited the activation of nuclear factor-kappa B and signal transducer and activator of transcription (STAT) 3 and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and cyclin D1 in the mouse colon. Further, oligonol inhibited azoxymethane-initiated and DSS-promoted adenoma formation in the mouse colon. Oligonol administration also attenuated lipid peroxidation (malondialdehyde) and protein oxidation (4-hydroxy-2-nonenal), thereby preventing oxidative stress-induced apoptosis of colonic epithelial cells. In vitro studies demonstrated that oligonol treatment reduced lipopolysaccharide-induced expression of interleukin (IL)-1 beta, tumor necrosis factor a, il-6, cox-2, and inos in murine macrophage RAW 264.7 cells. In another study, oligonol upregulated the antioxidant gene expression in the intestinal epithelial CCD841CoN cells and in the mouse colon. Innovation: Oligonol, an innovative formulation of catechin-type oligomers derived from the lychee fruit extract, was tested in this study for the first time to evaluate its effects on experimentally induced colitis and colonic adenoma formation in mice. Conclusion: Oligonol is effective in protecting against DSS-induced mouse colitis and colon carcinogenesis, suggesting that this polyphenol formulation may have a potential for the amelioration of inflammatory bowel disease and related disorders. Antioxid. Redox Signal. 19, 102-114.
ISSN
1523-0864
URI
https://hdl.handle.net/10371/172557
DOI
https://doi.org/10.1089/ars.2012.4626
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Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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