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

Autor: Min Woo Kim, Yeo Sung Yoon, Sun Yeou Kim, Ju-Hee Kang, Seung Hyun Oh, Seung-Ho Choi
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Lipopolysaccharides
0301 basic medicine
Wasabia
colitis
tight junction
mucin 2 (MUC2)
Mucin 2
Pharmacology
Inflammatory bowel disease
lcsh:Chemistry
Mice
chemistry.chemical_compound
Isothiocyanates
Wasabia japonica
lcsh:QH301-705.5
Spectroscopy
Barrier function
Tight junction
goblet cell
Dextran Sulfate
General Medicine
Allyl isothiocyanate
Computer Science Applications
dextran sodium sulfate (DSS)
Female
MAP Kinase Signaling System
digestive system
Article
Catalysis
Tight Junctions
Inorganic Chemistry
03 medical and health sciences
mucin
In vivo
medicine
Animals
Humans
Physical and Theoretical Chemistry
Colitis
Molecular Biology
Mucin-2
allyl isothiocyanate (AITC)
Organic Chemistry
Mucin
Inflammatory Bowel Diseases
medicine.disease
digestive system diseases
RAW 264.7 Cells
030104 developmental biology
Gene Expression Regulation
chemistry
lcsh:Biology (General)
lcsh:QD1-999
intestinal epithelial barrier
Caco-2 Cells
Zdroj: International Journal of Molecular Sciences, Vol 19, Iss 7, p 2025 (2018)
International Journal of Molecular Sciences
Volume 19
Issue 7
ISSN: 1422-0067
Popis: 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.
Databáze: OpenAIRE
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