Octacosanol Attenuates Inflammation in Both RAW264.7 Macrophages and a Mouse Model of Colitis

被引:164
|
作者
Guo, Tianyi [1 ]
Lin, Qinlu [1 ]
Li, Xinhua [2 ]
Nie, Ying [1 ]
Wang, Long [1 ]
Shi, Limin [1 ]
Xu, Wei [1 ]
Hu, Tao [1 ]
Guo, Ting [1 ]
Luo, Feijun [1 ]
机构
[1] Cent South Univ Forestry & Technol, Coll Food Sci & Engn, Natl Engn Lab Rice & Byprod, Lab Mol Nutr, Changsha 410004, Hunan, Peoples R China
[2] Cent S Univ, Xiangya Hosp, Dept Gastroenterol, Changsha 410008, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
octacosanol; colitis; inflammation factor; MAPK; NF-kappa B; AP-1; NF-KAPPA-B; CHRONIC ULCERATIVE-COLITIS; ACID-INDUCED COLITIS; BOWEL-DISEASE; NITRIC-OXIDE; OXIDATIVE STRESS; MOLECULAR-BASIS; CROHNS-DISEASE; P38; MAPK; MICE;
D O I
10.1021/acs.jafc.6b05465
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Octacosanol has multiple biological functions. In this study, the anti-inflammatory effect and molecular mechanism of octacosanol were evaluated by using dextran sulfate sodium (DSS)-induced ulcerative colitis model in mice and lipopolysaccharide (LPS)-stimulated mouse macrophage RAW264.7 cells. The colitis mouse model was induced by 3.0% DSS in 8-week ICR mice and octacosanol orally administered with 100 mg/kg/day. The results showed that octacosanol significantly improved the health status of mice and reduced DSS-induced pathological damage in the colonic tissues. Octacosanol obviously inhibited the mRNA and protein expression levels of pro-inflammatory factors of colonic tissues. In vitro, octacosanol administration significantly reduced the expression of mRNA or protein of pro-inflammatory cytokines and the phosphorylation of c-Jun N-terminal kinase and p38, and it also partly prevented LPS-induced translocations of NF-kappa B and AP-1. Octacosanol has anti-inflammatory effect, and its molecular mechanism may be involved in downregulating the expression of inflammatory factors and blocking of MAPK/NF-KB/AP-1 signaling pathway.
引用
收藏
页码:3647 / 3658
页数:12
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