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.