Literature DB >> 32468499

Alpha-Linolenic Acid Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice.

Jeongtae Kim1,2, Meejung Ahn1,3, Yuna Choi1, Taeyoung Kang1, Jungeun Kim4, Nam Ho Lee4, Gi Ok Kim5, Taekyun Shin6.   

Abstract

Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by inflammation of the large intestine, rectal bleeding, and abdominal pain. It can be alleviated by certain bioactive compounds, including α-linolenic acid (ALA), which is a bioactive component in fermented black radish (Raphanus sativus L. var. niger). The aim of this study was to evaluate the anti-inflammatory effects of ALA in dextran sulfate sodium (DSS)-induced UC in mice. UC was induced in C57BL/6 mice by allowing them to freely drink water containing 2.5% DSS for 7 days, followed by oral administration of ALA (30 and 60 mg/kg/day) or vehicle control for 7 days. DSS-induced colitis was evaluated using the Disease Activity Index (DAI) and by measuring colon length and performing a histopathological examination. Compared to the control group, the vehicle-treated group showed a higher DAI score, shorter colon, goblet cell loss, and crypt shortening. The ALA treatment mitigated clinical signs of UC and histopathological changes. Furthermore, it mitigated intestinal inflammation by reducing the expression of ionized calcium binding adaptor molecule 1-positive macrophages in the colon. These results show that ALA alleviates DSS-induced UC by suppressing colon damage, which includes goblet cell loss, crypt shortening, and a reduction of macrophages in the colon.

Entities:  

Keywords:  alpha-linolenic acid; colitis; dextran sulfate sodium; fermented black radish; inflammatory bowel disease; macrophages

Year:  2020        PMID: 32468499     DOI: 10.1007/s10753-020-01260-7

Source DB:  PubMed          Journal:  Inflammation        ISSN: 0360-3997            Impact factor:   4.092


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Review 10.  Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis.

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