Isoliquiritigenin ameliorates dextran sulfate sodium-induced colitis through the inhibition of MAPK pathway
- Authors
- Choi, Young Hee; Bae, Jin-Kyung; Chae, Hee-Sung; Choi, Young Ok; Nhoek, Piseth; Choi, Jong-Sun; Chin, Young-Won
- Issue Date
- Feb-2016
- Publisher
- ELSEVIER
- Keywords
- Isoliquiritigenin; Inflammatory bowel disease; MAPK inhibition; Colon
- Citation
- INTERNATIONAL IMMUNOPHARMACOLOGY, v.31, pp 223 - 232
- Pages
- 10
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- INTERNATIONAL IMMUNOPHARMACOLOGY
- Volume
- 31
- Start Page
- 223
- End Page
- 232
- URI
- https://scholarworks.dongguk.edu/handle/sw.dongguk/23446
- DOI
- 10.1016/j.intimp.2015.12.024
- ISSN
- 1567-5769
1878-1705
- Abstract
- Isoliquiritigenin (isoLQ), a chalcone found in licorice, has shown a variety of biological activity including antiinflammatory and antioxidative effects, and the distribution of isoLQ in gastrointestinal tract was higher than any other tissues. Thus, we evaluated whether or not isoLQ attenuated the dextran sulfate sodium (DSS)-induced colitis by observing the physiological changes (body weight loss, diarrhea, bleeding stool, overall disease activity index (DAI) scores, colon length), histopathological analysis and myeloperoxidase (MPO) activities of esophagus and colon. Also, the MAPK pathways including phosphorylation of ERK1/2, p38, and AKT, and the activation of NK-kappa B were evaluated in colon tissue. Interestingly, the reduction of body weight and colon length, increase of diarrhea, bloody stool, DAI scores and MPO activity, and histologic disturbances in DSS-induced colitis were recovered by isoLQ treatment. Also, isoLQ treatment suppressed the phosphorylation of ERK1/2 and p38, and the activation of NK-kappa B compared to those in DSS-induced colitis mice. In addition, the distributions of isoLQ in colon were relatively higher in DSS-induced colitis models. All of these results suggested that isoLQ has potential activity to ameliorate the DSS-induced colitis through the inhibition of MAPK pathway. (C) 2015 Elsevier B.V. All rights reserved.
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