Chinese yam polysaccharide attenuates DSS-induced ulcerative colitis by modulating gut microbiota and eicosanoid metabolism

This study investigated the protective mechanisms of Chinese yam polysaccharide (CYP) against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice, focusing on intestinal barrier repair, gut microbiota-mediated effects, and host lipid metabolic regulation. CYP treatment alleviated disease severity and restored colon length and histological structure, but did not significantly attenuate DSS-induced body weight loss. It upregulated ZO-1, occludin, and MUC-2, enhanced antioxidant enzyme activities, and reduced myeloperoxidase activity. Western blot analysis further demonstrated that CYP inhibited MAPK and NF-κB signaling pathways in colonic tissue, thereby reducing mucosal inflammation and alleviating hepatic oxidative stress. Furthermore, CYP supplementation modulated the gut microbiota by altering the relative abundances of key genera, including Bacteroides and Prevotella, and enhanced short-chain fatty acid production. Fecal microbiota transplantation (FMT) from CYP-treated donors partially reproduced the protective effects on histology in recipient mice, suggesting that gut microbiota may contribute to CYP-mediated protection. However, FMT did not significantly improve body weight, disease activity index, or colon length, indicating that the transferable protective effects were limited primarily to local histological improvement rather than full clinical recovery. Additionally, FMT did not significantly restore hepatic levels of the anti-inflammatory eicosanoids 18-HEPE and 13(14)-DiHDPA, whereas direct CYP administration markedly increased these metabolites. These results indicate that CYP-induced recovery of hepatic eicosanoid metabolism was not transferable through FMT. Overall, these findings suggest that CYP alleviates experimental colitis through a dual mechanism involving microbiota-associated immunoregulation and microbiota-independent host lipid metabolic modulation, providing mechanistic insight into the multi-level protective actions of CYP in UC.