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

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.

Curcumin and Its Modified Formulations on Inflammatory Bowel Disease (IBD): The Story So Far and Future Outlook

“…The intestinal tight junction’s protein complexes link the atypical membranes between intestinal epithelial cells and act as a physical barrier, giving selective permeability. Deficiencies in tight junctions result in increased gut permeability, leading to an increased entrance of luminal antigens and contributing to intestinal inflammation [ 8 ]. IBD is one of the two most widespread diseases reflecting immune dysfunction, and another one is rheumatoid arthritis.…”

Effect of N‐palmitoylethanolamine‐oxazoline on comorbid neuropsychiatric disturbance associated with inflammatory bowel disease

“…Defects in the tight junctions result in increased gut permeability, which leads to an increased entrance of luminal antigens and contributes to intestinal inflammation. 1 Recent studies using an animal model of IBD induced by dextran sulfate sodium (DSS) administration have demonstrated not only activation of the inflammatory pathway, oxidative stress, and the alteration in serotonin (5-hydroxytryptamine )-producing enterochromaffin cells (EC), as are well known, but also anxiety-like and depressive-like behavior, cognitive impairment and decreased social interactions. [2][3][4][5][6] One of the most supported ideas linked IBD with central nervous system (CNS) neuroinflammation.…”

Allyl Isothiocyanate Protects Acetaminophen-Induced Liver Injury via NRF2 Activation by Decreasing Spontaneous Degradation in Hepatocyte

“…In our previous work, we reported the protective effect of AITC on intestinal epithelium in DSS-induced colitis model via increasing the tight junction and mucin expression [ 8 ]. In this study, we endeavored to examine another beneficial effect of AITC, by investigating the effects of AITC on liver.…”

“…Recent papers have further reported that the microbiota metabolizes glucosinolates into isothiocyanates such as AITC [ 6 , 7 ], highlighting the importance of the dietary intake of Cruciferae plants and the function of isothiocyanates in the human body. Previously, we reported the beneficial effects of AITC on intestinal epithelium in the dextran sulfate sodium (DSS)-induced colitis model [ 8 ]. In the current study, we intend to further study the function of AITC in liver, since the absorbed AITC first enters the liver via portal circulation and is mainly metabolized here [ 9 ].…”