Echinacea Purpurea Polysaccharides Alleviate DSS-Induced Colitis in Rats by Regulating Gut Microbiota and Short-Chain Fatty Acid Metabolism

TL;DR

Echinacea purpurea polysaccharides reduce colitis in rats by improving gut bacteria and short-chain fatty acid levels.

Contribution

EPP's therapeutic mechanism is linked to the microbiota-metabolite-host axis in IBD.

Findings

EPP reduces pro-inflammatory cytokines and inhibits TRAF6/NF-κB signaling in IBD rats.

EPP restores gut microbiota balance by increasing Bacteroidetes and decreasing Firmicutes.

Co-housed rats with EPP treatment show reduced disease activity and inflammation without antibiotics.

Abstract

To investigate whether Echinacea purpurea polysaccharides (EPP) alleviate inflammatory bowel disease (IBD) by modulating gut microbiota, we utilized a mixed antibiotic (ABX)-induced gut dysbiosis model and a co-housing model in rats. ABX treatment severely reduces microbial richness and functional diversity, decreasing SCFA-producing bacteria and impairing the anti-inflammatory effect of SCFA-mediated EPP. Without ABX, EPP significantly ameliorates IBD symptoms and colonic pathology damage in rats, reduces the levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) (p < 0.05), inhibits the activation of the TRAF6/NF-κB signaling pathways, and reverses gut microbiota imbalance by partially restoring Bacteroidetes abundance and reducing Firmicutes levels. Among co-housed rats, the EPP-treated group exhibited significantly lower Disease Activity Index (DAI) scores, serum levels of pro-inflammatory factors, and colonic expression of pro-inflammatory pathway-related gene (TRAF6, STAT3) (p < 0.05) without ABX. 16S rRNA gene sequencing revealed a significant reduction in Firmicutes abundance (p < 0.05) alongside significant increases in Bacteroidetes and Actinobacteria abundances, accompanied by elevated levels of acetic acid and propionic acid (p < 0.05). These findings suggest recipient mice restored microbial function and acquired IBD-regulating ability post-microbial exchange. EPP alleviates IBD-related pathological injury by inhibiting the JAK2/STAT3 and TRAF6/NF-κB signaling pathways, with its therapeutic mechanism intricately linked to the microbiota–metabolite–host axis.

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