# 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.

## Key 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.