Rattan Pepper Polysaccharide Regulates DSS-Induced Intestinal Inflammation and Depressive Behavior through Microbiota–Gut–Brain Axis

Inflammatory bowel disease (IBD) is a chronic and recurrent disease. Increasing evidence suggests a higher incidence of depression in IBD patients compared with the general population, but the underlying mechanism remains uncertain. Rattan pepper polysaccharide (RPP) is an important active ingredien...

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Published in:Journal of agricultural and food chemistry 2024-01, Vol.72 (1), p.437-448
Main Authors: Chang, Lili, Wang, Chendi, Peng, Jing, Song, Yujie, Zhang, Wanting, Chen, Yurui, Peng, Qiang, Li, Xiulian, Liu, Xuebo, Lan, Ying
Format: Article
Language:English
Subjects:
Animals
Bioactive Constituents, Metabolites, and Functions
Brain-Gut Axis
Colitis - chemically induced
Colitis - drug therapy
Colon
Dextran Sulfate - adverse effects
Disease Models, Animal
Humans
Inflammation - drug therapy
Inflammatory Bowel Diseases
Mice
Mice, Inbred C57BL
Piper nigrum
Sodium Chloride
Sodium Chloride, Dietary
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Summary:Inflammatory bowel disease (IBD) is a chronic and recurrent disease. Increasing evidence suggests a higher incidence of depression in IBD patients compared with the general population, but the underlying mechanism remains uncertain. Rattan pepper polysaccharide (RPP) is an important active ingredient of rattan pepper, yet its effects and mechanisms on intestinal inflammation and depression-like behavior remain largely unknown. This study aims to investigate the ameliorating effect of RPP on dextran sulfate sodium salt (DSS)-induced intestinal inflammation and depression-like behavior as well as to reveal its mechanism. Our results indicate that RPP effectively ameliorated intestinal microbiota imbalance and metabolic disorders of short-chain fatty acids (SCFAs) and bile acids in mice with DSS-induced inflammation, contributing to the recovery of intestinal Th17/Treg homeostasis. Importantly, RPP effectively alleviated brain inflammation caused by intestinal inflammatory factors entering the brain through the blood–brain barrier. This effect may be attributed to the inhibition of the TLR4/NF-κB signaling pathway, which alleviates neuroinflammation, and the activation of the CREB/BDNF signaling pathway, which improves synaptic dysfunction. Therefore, our findings suggest that RPP may play a role in alleviating DSS-induced gut inflammation and depression-like behavior through the microbiota–gut–brain axis.
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.3c08462