关键词: 肠道菌群代谢产物, 吲哚乙酸, 溃疡性结肠炎, 芳香烃受体, 炎症反应, 免疫平衡, 色氨酸

Abstract:

The aim of this study is to investigate the mechanism action of indole acetylated high-amylose maize starch in improving ulcerative colitis. Dextran sulfate sodium salt was used to induce acute ulcerative colitis in mice. Indole acetylated high-amylose maize starch was then used to target the colon with the delivery of indole-3-acetic acid. This was combined with the administration of an aryl hydrocarbon receptor inhibitor to analyze the mice in terms of colon length; disease activity index; and levels of interleukin-6, interleukin-10, transforming growth factor β1, myeloperoxidase, and interleukin-22 in the colon, which were detected by enzyme-linked immunosorbent assay. Quantitative polymerase chain reaction was used to analyze the relative expression levels of the colonic tight junction proteins occludin, ZO-1, and CYP1A1. Flow cytometry was used to test the ratio of regulatory T cells and T helper 17 cells in the mesenteric lymph nodes. The results showed that administration of indole acetylated high-amylose maize starch significantly alleviated the shortening of the colon length; significantly reduced the disease activity index and the levels of interleukin-6 and myeloperoxidase; significantly promoted the expression of interleukin-10, transforming growth factor β1, interleukin-22, CYP1A1, occludin, and ZO-1; significantly increased the proportion of regulatory T cells; and significantly reduced the proportion of T helper 17 cells. Administration of the aryl hydrocarbon receptor inhibitor weakened the effect of indole acetylated high-amylose maize starch. These results together suggest that acetylated high-amylose maize starch can improve ulcerative colitis by activating aryl hydrocarbon receptors.

Key words: microbiota metabolites, indole-3-acetic acid, ulcerative colitis, aryl hydrocarbon receptors, inflammatory response, immune balance, tryptophan