Gut barrier dysfunction is triggered by gut microbiota dysbiosis that is closely associated with ulcerative colitis. Recently, more attention has been devoted to the ability of the non-digestively colon-targeted plant polysaccharides to regulate the function and composition of the intestinal microbiota. Here, we first studied the prophylactic capacity of turmeric polysaccharides (TPS) to ameliorate dextran sulfate sodium (DSS)-induced gut microbiota imbalance. The results revealed that TPS administration could greatly improve the pathological phenotype, gut barrier disruption and colon inflammation in colitis mice. Besides, targeted metabolomics or 16S rRNA-based microbiota analysis demonstrated that TPS alleviated gut microbiota dysbiosis caused by DSS, especially increasing the abundance of probiotics associated with tryptophan metabolism, such as Lactobacillus and Clostridia-UCG-014, where the cecal tryptophan catabolite indole-3-acetic acid (IAA) and its ligand aryl hydrocarbon receptor (AhR) expressions were sharply increased by TPS treatment in colitis mice. Expectedly, TPS was found to exert its gut barrier functions through the activation of AhR to upregulate epithelial tight junction proteins. These findings highlight the protective effects of TPS against ulcerative colitis by modulating the gut microbiota and improving microbial metabolites and gut barrier function.

This study was designed to investigate the tumor-inhibitory effects of quercetin (Que) and its water-soluble metabolites, quercetin-3′-sulfate (Q3′S) and quercetin-3-glucuronide (Q3G), as well as to make the molecular mechanism and structure–antitumor relationship clear. It was found that Que, Q3′S, and Q3G could inhibit the growth of human breast cancer MCF-7 cells in a dose-dependent manner, with the IC₅₀ values of 23.1, 27.6, and 73.2 μM, respectively, and their anticancer effect was ranked as Que > Q3′S > Q3G. Furthermore, flow cytometric assay revealed that Que, Q3′S, and Q3G mediated the cell-cycle arrest principally at the S phase and decreased the number of G0/G1 and G2/M after a 48 h treatment with human breast MCF-7 cells. Moreover, it was found that 70.8%, 58.2%, and 48.0% of MCF-7 cancer cells entered the early phase of apoptosis when treated with 100 μM Que, Q3′S, and Q3G for 48 h, respectively. In addition, induction of apoptosis by Que, Q3′S, and Q3G was accompanied by marginal generation of intracellular reactive oxygen species (ROS) in the MCF-7 cancer cells. Overall, these results demonstrate that Que, Q3′S, and Q3G possess strong antitumor effects through induction of an ROS-dependent apoptosis pathway in MCF-7 cells.