Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 67, Issue 48, Pages 13282-13298Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.9b05744
Keywords
conjugated linoleic acid; colitis; intestinal barrier function; oxidative stress; gut microbiota
Funding
- National Natural Science Foundation of China [31801521, 31722041]
- Fundamental Research Funds for the Central Universities [JUSRP51702A]
- National First-Class Discipline Program of Food Science and Technology [JUFSTR20180102]
- Postgraduate Research and Practice Innovation Program of Jiangsu Province [CYCX19_1829]
- Wuxi Young Talent Foundation [QNRC075]
- Jiangsu Province Collaborative Innovation Center for Food Safety and Quality Control
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Dietary supplementation with conjugated linoleic acid (CLA) has been reported to alleviate the effect of colitis in mice, but the mechanisms involved need further exploration. The study aimed to investigate how orally administered CLA alleviates dextran sulfate sodium (DSS)-induced colitis in mice. CLA was administered in five different doses: 40, 20, 10, 5, and 2.5 mg/day. Doses of CLA at 10 mg/day and higher alleviated colitis symptoms and reduced inflammation induced by DSS, in which 40, 20, and 10 mg/day CLA significantly increased the concentration of mucin2 and goblet cells, but neither 5 mg/day CLA nor 2.5 mg/day CLA had any effects. Meanwhile, 40 and 20 mg/day CLA treatments significantly upregulated the concentration of tight junction proteins (ZO-1, occludin, and claudin-3) and ameliorated epithelial apoptosis caused by DSS. Moreover, oxidative-stress-related enzymes (superoxide dismutase, glutathione peroxidase, and catalase) and inflammatory cytokines [tumor necrosis factor-a, interleukin (IL)-10, and IL-6] were modulated by 40 and 20 mg/day CLA. Furthermore, 40 mg/day CLA rebalanced the gut microbiota damaged by DSS, including reducing Bacteroides and increasing Bifidobacterium and Odoribacter. In conclusion, CLA supplementation alleviated DSS-induced colitis in a dose-dependent manner by modulating inflammatory cytokines and oxidation stress, maintaining the mucosal barrier, and reverting microbiota changes.
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