Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice via NF-κB/MAPK Suppression and Gut Microbiota Modulation.

(CUM) possesses various biological effects, including anti-inflammatory, intestinal microbiota regulatory, and immunomodulatory activities. However, there has been little exploration regarding the effects of CUM on ulcerative colitis (UC). Therefore, this study aimed to investigate the beneficial effects of CUM on alleviating dextran sulfate sodium (DSS)-induced UC in mice and to explore the potential underlying mechanisms. Here, the effect of CUM on UC was analyzed using a DSS-induced colitis mouse model (n = 9), the results of which indicated a decrease in disease activity index (DAI) in DSS-induced UC mice. Furthermore, CUM alleviated colon shortening, minimized intestinal tissue damage, and preserved intestinal tight junction proteins (Claudin-3, Occludin, and ZO-1). CUM reduced the level of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), inhibited the activation of the NF-ĸB, MAPK and PPARγ signaling pathways, and decreased the level of oxidative mediators (MPO, SOD and MDA) in the colon of UC mice. Additionally, it mitigated the dysbiosis of intestinal microbiota in UC mice by increasing the abundance of and while decreasing the abundance of and . CUM alleviated the decrease in short-chain fatty acids (SCFAs) content in the colon of UC mice. The above results provide a scientific basis for CUM, as a natural supplement, to restore the balance of the gut inflammatory microbiota and promote gut health.