Dietary Turmeric Consumption Alleviates Ulcerative Colitis via Restoring Tryptophan Metabolism and Alleviating Gut Microbiota Dysbiosis in Mice,Journal of Agricultural and Food Chemistry

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Dietary Turmeric Consumption Alleviates Ulcerative Colitis via Restoring Tryptophan Metabolism and Alleviating Gut Microbiota Dysbiosis in Mice
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2022-11-22 , DOI: 10.1021/acs.jafc.2c04509
Chengcheng Yang ₁ , Yao Du ₁ , Aiqing Zhao ₁ , Lei Liu ₂ , Daoyuan Ren ₁ , Pengfei Niu ₁ , Xiangnan Zhang ₁ , Yu Wang ₁ , Yan Zhao ₂ , Xingbin Yang ₁

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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.

中文翻译：

食用姜黄可通过恢复色氨酸代谢和缓解小鼠肠道菌群失调来缓解溃疡性结肠炎

本研究旨在首先验证姜黄粉 (TP) 作为传统烹饪香料对葡聚糖硫酸钠 (DSS) 引起的肠道炎症和肠道菌群失衡的保护能力。DSS 诱导的小鼠被喂食添加或不添加 TP (8%) 的标准啮齿动物食物 37 天。结果表明，通过补充 TP，DSS 诱导的小鼠的病理表型、肠屏障破坏和结肠炎症得到显着改善。此外，基于 16S rRNA 的微生物群或靶向代谢组学分析表明，TP 改善了由 DSS 引起的肠道微生物群失调，特别是增加了与色氨酸代谢相关的益生菌的丰度，例如乳杆菌和双歧杆菌，其中盲肠色氨酸被代谢为吲哚-3-丙酸和吲哚-3-乙酸。摄入 TP 可显着提高结肠炎小鼠结肠芳香烃受体的表达水平，并进一步增加肠道紧密连接蛋白和白细胞介素 22 的表达。总的来说，这些发现通过恢复肠道微生物群紊乱、促进微生物代谢和改善肠道屏障损伤，证明了膳食 TP 摄入对溃疡性结肠炎的保护作用。

更新日期：2022-11-22

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