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Alliin protects against inflammatory bowel disease by preserving the gene expression in colonic epithelial cells rather than altering gut microbiota

[Display omitted] •Alliin prevents colon shortening caused by colitis.•Alliin relieves inflammation by lowering myeloperoxidase activity.•The protective effect of alliin does not attribute to gut microbiota alteration.•Alliin sustains the expression of 23 genes in colonic epithelial cells. Inflammat...

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Published in:Journal of functional foods 2019-08, Vol.59, p.309-318
Main Authors: Li, Xuanwei, Luo, Jianming, Zhang, Cheng, Liu, Liu, Ou, Shiyi, Zhang, Guangwen, Peng, Xichun
Format: Article
Language:English
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Summary:[Display omitted] •Alliin prevents colon shortening caused by colitis.•Alliin relieves inflammation by lowering myeloperoxidase activity.•The protective effect of alliin does not attribute to gut microbiota alteration.•Alliin sustains the expression of 23 genes in colonic epithelial cells. Inflammatory bowel disease (IBD) has affected an increasing number of people worldwide while alliin has antibiotic effects and is able to alleviate inflammation. We aim to figure out whether pre-consumption of alliin prevents IBD and better understand the mechanism. Rats were orally administrated with alliin prior to the dextran sulfate sodium (DSS)-induced colitis. The inflammatory status, profiles of gut microbial communities and colonic epithelial cells (CECs) gene expressions were also examined. Our results showed that alliin mitigated the inflammation symptom including colon shrinkage prevention, and leukocyte and neutrophil infiltration attenuation by preserving expression of 23 genes in CECs rather than altering gut microbiota. DSS induced the differentially expressed genes related to rodent immune system, while alliin obviate the DSS-induced pathological change through other systems rather than the immune one. The value and prospect of alliin as a prevention for colitis and the potential gene targets for treating IBD are discussed.
ISSN:1756-4646
2214-9414
DOI:10.1016/j.jff.2019.05.048