肠道菌群
MAPK/ERK通路
巴戟天属
丁酸
下调和上调
NF-κB
化学
炎症性肠病
药理学
生物
生物化学
信号转导
医学
传统医学
疾病
内科学
基因
作者
Mingyu Jin,Xiaoyong Wu,Meiying Li,Xiaotong Li,Riming Huang,Yuanming Sun,Zhen-Lin Xu
标识
DOI:10.1021/acs.jafc.1c03833
摘要
Inflammatory bowel disease (IBD) is a disease characterized by intestinal inflammation with immune dysregulation and intestinal microecological imbalance. In a dextran sulfate sodium salt (DSS)-induced IBD mouse model, noni (Morinda citrifolia L.) fruit polysaccharides (NFP) with homogalacturonan and rhamnogalacturonan-I domain decreased the concentration of serum LPS, TNF-α, and IL-17 by 84, 42, and 65%, respectively. It was abolished when intestinal microbiota were depleted by antibiotics. Sequencing analysis of gut microbiota showed an attenuated disruption of the microbial composition in the DSS+NFP group. Targeted metabolomic analysis revealed that NFP upregulated the content of acetic acid, propionic acid, and butyric acid by onefold but reduced isobutyric acid and isovaleric acid contents. NFP also inhibited JNK, ERK, and NF-κB phosphorylation of IBD mice. Taken together, the mechanism of NFP alleviating IBD is related to the intestinal microecological balance to inhibit inflammatory signaling pathways. This study provides a basis for NFP as a cheap intervention for the prevention and treatment of IBD patients.
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