期刊
CARBOHYDRATE POLYMERS
卷 219, 期 -, 页码 269-279出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.carbpol.2019.05.036
关键词
Chitosan oligosaccharide (COS); Inflammation; IPEC-J2; TLE4/NE-kappa B
资金
- National Natural Science Foundation of China [31101862, 31472243]
- Project of Science and Technology Plan of Guangdong Province [2015A020216019, 2017A010103023]
- Shenzheng Projects for Basic Research [JCYJ20170306162414058]
- Project of Enhancing School With Innovation of Guangdong Ocean University [GDOU2013050221, GDOU20160502 55]
The protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharides (LPS) -induced inflammatory responses in IPEC-J2 and in mice with DSS dextran sulfate sodium (DSS) -induced colitis is reported. Upon exposure to LPS, the proliferation rate of IPEC-J2 cells markedly decreased, and epithelial cell integrity was compromised. However, COS pretreatment significantly reduced these changes. Low-concentration (200 mu g/mL) COS up-regulated Toll-like receptor 4 (TLR4) and nuclear p65 expression, but inhibited LPS-induced expression of nuclear p65, IL-6, and IL-8. Addition of the TLR4 inhibitor reduced nuclear p65, IL-6, and IL-8 expression in IPEC-J2 cells exposed to COS or LPS alone, and a slight up-regulation in nuclear p65 was observed in COS and LPS co-treated cells. Medium-dose COS (600 mg/kg/d) protected against DSS-induced colitis, in which TLR4 and nuclear p65 expression levels were decreased. We postulate that the prevention of both LPS- and DSS -induced inflammatory responses in IPEC-J2 cells and mice by COS are related to the inhibition of the TLR4/NF-kappa B signaling pathway.
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