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Allyl Isothiocyanate Ameliorates Dextran Sodium Sulfate-Induced Colitis in Mouse by Enhancing Tight Junction and Mucin Expression

Authors
Kim, Min WooChoi, SeunghoKim, Sun YeouYoon, Yeo SungKang, Ju-HeeOh, Seung Hyun
Issue Date
Jul-2018
Publisher
MDPI
Keywords
allyl isothiocyanate (AITC); Wasabia japonica; intestinal epithelial barrier; tight junction; mucin; mucin 2 (MUC2); goblet cell; dextran sodium sulfate (DSS); colitis
Citation
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.19, no.7
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume
19
Number
7
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3627
DOI
10.3390/ijms19072025
ISSN
1422-0067
Abstract
Inflammatory bowel disease (IBD) is characterized by chronic or recurrent inflammation of the gastrointestinal tract. Even though the current strategies to treat IBD include anti-inflammatory drugs and immune modulators, these treatments have side-effects. New strategies are, therefore, required to overcome the limitations of the therapies. In this study, we investigated the anti-colitic effects of allyl isothiocyanate (AITC), which is an active ingredient present in Wasabia japonica. The DSS-induced colitis model in the mouse was used to mimic human IBD and we observed that AITC treatment ameliorated the severity of colitis. We further studied the mechanism involved to ameliorate the colitis. To investigate the involvement of AITC on the intestinal barrier function, the effect on the intercellular tight junction was evaluated in the Caco-2 cell line while mucin expression was assessed in the LS174T cell line. AITC positively regulated tight junction proteins and mucin 2 (MUC2) against DSS-induced damage or depletion. Our data of in vivo studies were also consistent with the in vitro results. Furthermore, we observed that MUC2 increased by AITC is dependent on ERK signaling. In conclusion, we propose that AITC can be considered as a new strategy for treating IBD by modulating tight junction proteins and mucin.
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