This study was designed to first verify the protective capacity of turmeric powder (TP) as a traditional cooking spice against dextran sulfate sodium (DSS)-induced intestinal inflammation and intestine microbiota imbalance. The DSS-induced mice were fed a standard rodent chow supplemented with or without TP (8%) for 37 days. The results indicated that the pathological phenotype, gut barrier disruption, and colon inflammation of DSS-induced mice were significantly improved through supplementation of TP. In addition, 16S rRNA-based microbiota or targeted metabolomics analysis indicated that TP ameliorated intestinal microbiota dysbiosis caused by DSS and particularly enhanced the abundances of probiotics correlated with tryptophan metabolism, such as Lactobacillus and Bifidobacterium, where the cecal tryptophan was metabolized to indole-3-propionic acid and indole-3-acetic acid. Consumption of TP markedly enhanced the expression levels of colonic aromatic hydrocarbon receptors and further increased the expressions of intestinal tight junction proteins and interleukin-22 in the colitis mice. Collectively, these findings manifest the protective actions of dietary TP consumption against ulcerative colitis via restoring the intestinal microbiota disorders, promoting microbial metabolism, and improving intestinal barrier damage.
Keywords: gut barrier function; gut microbiota; tryptophan catabolites; turmeric powder; ulcerative colitis.