The protective role of Chitooligosaccharides against chronic ulcerative colitis induced by dextran sulfate sodium in mice

被引:12
作者
Guo, Jie
Liao, Mengfan
Zhu, Yujie
Hu, Xianmin
Wang, Jun [1 ]
机构
[1] Wuhan Univ Sci & Technol, Hubei Prov Key Lab Occupat Hazard Identificat & C, Wuhan 430065, Peoples R China
基金
中国国家自然科学基金;
关键词
Chitooligosaccharides; Chronic; Mechanisms; Reg3g; TLR4; Ulcerative colitis; INFLAMMATORY-BOWEL-DISEASE; CHITOSAN OLIGOSACCHARIDES; INTESTINAL MICROBIOTA; BIOLOGICAL-ACTIVITIES; EXPRESSION; DIET; GLUCOSAMINE; APOPTOSIS; FAMILY; CELLS;
D O I
10.1016/j.jff.2021.104809
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Chitooligosaccharides(COS) as potential functional food has been paid great attention because of their outstanding biological activities. Here, we found COS (250 and 500 mg/kg) protected against development of dextran sodium sulfate(DSS)- induced chronic experimental ulcerative colitis(UC) in mice. DSS-elevated serum and colonic tumor necrosis factor(TNF)-alpha, interleukin(IL)-1 beta and IL-6 levels were significantly supressed. TUNEL+ apoptoic cells and Cleaved Caspase-9 expression were downregulated, Ki-67(+) proliferative cells in colonic crypts and Bcl-2/Bax ratio were upregulated in COS-treated colons compared to DSS controls. COS enhanced gut microbiota diversity and restored community structure in chronic UC mice. Colonic expression of TLR4, NF-kappa B, STAT3 and pSTAT3 was significantly decreased, but that of regenerating islet derived 3 gamma (Reg3g) was increased by COS. Overall, COS represents a treatment alternative in chronic UC management via ameliorating inflammation, promoting mucosal repair and modulating gut microbiota. Inhibition of TLR4 signal and induction of colonic Reg3g might be involved in molecular mechanisms.
引用
收藏
页数:11
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