溃疡性结肠炎
TLR4型
结肠炎
化学
下调和上调
肿瘤坏死因子α
炎症
标记法
车站3
药理学
免疫学
细胞凋亡
癌症研究
内科学
生物化学
医学
基因
疾病
作者
Jie Guo,Mengfan Liao,Yujie Zhu,Xianmin Hu,Jun Wang
标识
DOI:10.1016/j.jff.2021.104809
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)-α, interleukin(IL)-1β 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-κB, 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.
科研通智能强力驱动
Strongly Powered by AbleSci AI