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杨梅素通过作用于肠道微生物群产生丁酸来缓解 DSS 诱导的溃疡性结肠炎。

Taxifolin Alleviates DSS-Induced Ulcerative Colitis by Acting on Gut Microbiome to Produce Butyric Acid.

机构信息

College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.

出版信息

Nutrients. 2022 Mar 3;14(5):1069. doi: 10.3390/nu14051069.

Abstract

Taxifolin is a bioflavonoid which has been used to treat Inflammatory Bowel Disease. However, taxifolin on DSS-induced colitis and gut health is still unclear. Here, we studied the effect of taxifolin on DSS-induced intestinal mucositis in mice. We measured the degree of intestinal mucosal injury and inflammatory response in DSS treated mice with or without taxifolin administration and studied the changes of fecal metabolites and intestinal microflora using 16S rRNA. The mechanism was further explored by fecal microbiota transplantation. The results showed that the weight loss and diarrhea score of the mice treated with taxifolin decreased in DSS-induced mice and longer colon length was displayed after taxifolin supplementation. Meanwhile, the expression of GPR41 and GPR43 in the colon was significantly increased by taxifolin treatment. Moreover, the expression of TNF-α, IL-1β, and IL-6 in colon tissue was inhibited by taxifolin treatment. The fecal metabolism pattern changed significantly after DSS treatment, which was reversed by taxifolin treatment. Importantly, taxifolin significantly increased the levels of butyric acid and isobutyric acid in the feces of DSS-treated mice. In terms of gut flora, taxifolin reversed the changes of , and further decreased . Fecal transplantation from taxifolin-treated mice showed a lower diarrhea score, reduced inflammatory response in the colon, and reduced intestinal mucosal damage, which may be related to the increased level of butyric acid in fecal metabolites. In conclusion, this study provides evidence that taxifolin can ameliorate DSS-induced colitis by altering gut microbiota to increase the production of SCFAs.

摘要

山奈酚是一种生物类黄酮,已被用于治疗炎症性肠病。然而,山奈酚对 DSS 诱导的结肠炎和肠道健康的影响尚不清楚。在这里,我们研究了山奈酚对 DSS 诱导的小鼠肠道黏膜炎的影响。我们测量了 DSS 处理的小鼠中肠道黏膜损伤和炎症反应的程度,以及用 16S rRNA 研究粪便代谢物和肠道微生物群的变化。通过粪便微生物群移植进一步探讨了机制。结果表明,在 DSS 诱导的小鼠中,用山奈酚处理的小鼠体重减轻和腹泻评分降低,并且补充山奈酚后结肠长度更长。同时,山奈酚处理显著增加了结肠中 GPR41 和 GPR43 的表达。此外,山奈酚处理抑制了结肠组织中 TNF-α、IL-1β 和 IL-6 的表达。DSS 处理后粪便代谢模式发生显著变化,山奈酚处理可逆转这种变化。重要的是,山奈酚显著增加了 DSS 处理小鼠粪便中丁酸和异丁酸的水平。就肠道菌群而言,山奈酚逆转了 的变化,并进一步降低了 。来自山奈酚处理小鼠的粪便移植显示出较低的腹泻评分、结肠中炎症反应降低和肠道黏膜损伤减少,这可能与粪便代谢物中丁酸水平升高有关。总之,这项研究提供了证据表明,山奈酚可以通过改变肠道微生物群来增加 SCFAs 的产生,从而改善 DSS 诱导的结肠炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba50/8912346/5e0502a5e50f/nutrients-14-01069-g001.jpg

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