化学
脂多糖
结肠炎
丁酸盐
肠道菌群
一氧化氮
丁酸钠
炎症性肠病
药理学
生物化学
生物
免疫学
内科学
医学
有机化学
基因
发酵
疾病
作者
Congcong Guo,Yue Zhang,Ling Tao,Chongjie Zhao,Yanru Li,Meng Geng,Sailun Gai,Wei Qi,Xue‐Gang Luo,Liehuan Chen,Tongcun Zhang,Nan Wang
出处
期刊:Marine Drugs
[Multidisciplinary Digital Publishing Institute]
日期:2022-01-24
卷期号:20 (2): 96-96
被引量:21
摘要
Chitosan oligosaccharides (COS) have been shown to have potential protective effects against colitis, but the mechanism underlying this effect has not been fully elucidated. In this study, COS were found to significantly attenuate dextran sodium sulfate-induced colitis in mice by decreasing disease activity index scores, downregulating pro-inflammatory cytokines, and upregulating Mucin-2 levels. COS also significantly inhibited the levels of nitric oxide (NO) and IL-6 in lipopolysaccharide-stimulated RAW 264.7 cells. Importantly, COS inhibited the activation of the NF-κB signaling pathway via activating PPARγ and SIRT1, thus reducing the production of NO and IL-6. The antagonist of PPARγ could abolish the anti-inflammatory effects of COS in LPS-treated cells. COS also activated SIRT1 to reduce the acetylation of p65 protein at lysine 310, which was reversed by silencing SIRT1 by siRNA. Moreover, COS treatment increased the diversity of intestinal microbiota and partly restored the Firmicutes/Bacteroidetes ratio. COS administration could optimize intestinal microbiota composition by increasing the abundance of norank_f_Muribaculaceae, Lactobacillus and Alistipes, while decreasing the abundance of Turicibacte. Furthermore, COS could also increase the levels of propionate and butyrate. Overall, COS can improve colitis by regulating intestinal microbiota and the PPARγ/SIRT1-mediated NF-κB pathway.
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