文献类型：期刊文献

英文题名：Chitosan oligosaccharide-mediated attenuation of LPS-induced inflammation in IPEC-J2 cells is related to the TLR4/NF-kappa B signaling pathway

作者：Shi, Lin[1,5];Fang, Biao[1];Yong, Yanhong[2];Li, Xuewen[2];Gong, Dongliang[2];Li, Junyu[1];Yu, Tianyue[1];Gooneratne, Ravi[3];Gao, Zhenhua[1];Li, Sidong[4];Ju, Xianghong[2,5]

机构：[1]Guangdong Ocean Univ, Dept Anim Sci, Coll Agr Sci, Zhanjiang 524088, Guangdong, Peoples R China;[2]Guangdong Ocean Univ, Dept Vet Med, Coll Agr Sci, Zhanjiang 524088, Guangdong, Peoples R China;[3]Lincoln Univ, Dept Wine Food & Mol Biosci, Fac Agr & Life Sci, Lincoln 7647, New Zealand;[4]Guangdong Ocean Univ, Coll Chem & Environm, Zhanjiang 524088, Guangdong, Peoples R China;[5]Guangdong Ocean Univ, Shenzhen Inst, Shenzhen 518018, Peoples R China

年份：2019

卷号：219

起止页码：269

外文期刊名：CARBOHYDRATE POLYMERS

收录：SCI-EXPANDED(收录号：WOS:000469334500029)、、EI(收录号：20192106950543)、Scopus(收录号：2-s2.0-85065756164)、WOS

基金：Xianghong Ju, Zhenhua Gao, Sidong Li, and Ravi Gooneratne contributed to conception, design, and edited the paper; Lin Shi conducted research, analyzed data, and performed statistical analyses. Lin Shi, Biao Fang, Xuewen Li, Yanhong Yong, Dongliang Gong, Junyu Li, and Tianyue Yu wrote the paper and have primary responsibility for the final content. All authors read and approved the final manuscript.; This study was supported by the National Natural Science Foundation of China [grant nos. 31101862, 31472243], Project of Science and Technology Plan of Guangdong Province (2015A020216019, 2017A010103023), Shenzheng Projects for Basic Research [JCYJ20170306162414058], and Project of Enhancing School With Innovation of Guangdong Ocean University (GDOU2013050221, GDOU20160502 55).

语种：英文

外文关键词：Chitosan oligosaccharide (COS); Inflammation; IPEC-J2; TLE4/NE-kappa B

外文摘要：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.