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黄山花菇多糖通过调节肠道微生物群依赖的 Th17/Treg 平衡改善葡聚糖硫酸钠诱导的结肠炎。

Huangshan Floral Mushroom Polysaccharide Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice by Modulating Th17/Treg Balance in a Gut Microbiota-Dependent Manner.

机构信息

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, Hefei, 230009, China.

School of Food and Biological Engineering, Hefei University of Technology, Hefei, 230009, China.

出版信息

Mol Nutr Food Res. 2023 Jan;67(2):e2200408. doi: 10.1002/mnfr.202200408. Epub 2022 Dec 5.

Abstract

SCOPE

Ulcerative colitis (UC) is a common chronic recurrent inflammatory bowel disease. This study attempts to reveal the improvement mechanism of floral mushroom polysaccharide (FMPS) on UC from the perspective of coordinated interaction between intestinal microbes and intestinal helper T cell 17 (Th17)/regulatory T cell (Treg) balance.

METHODS AND RESULTS

Dextran sulfate sodium (DSS)-induced colitis mice model is used for the experiment. The results suggest that FMPS up-regulated the expression of occludin, ZO-1, and MUC2, and down-regulated the secretion of TNF-α, IL-1β, and IL-6 in colitis mice. Importantly, FMPS restores intestinal Th17/Treg balance. Meanwhile, FMPS can regulate intestinal microorganisms and improve the level of short-chain fatty acids (SCFAs) in colitis mice. Intestinal microbial depletion and fecal microbiota transplantation (FMT) experiments reveal that FMPS ameliorated UC is mediated by intestinal microbiome. Flow cytometry further proves that FMPS restores intestinal Th17/Treg balance in a microbial-dependent manner.

CONCLUSION

These results indicate that FMPS has the potential to improve UC, and its mechanism depends on the restoration of Th17/Treg balance mediated by intestinal microorganisms. Therefore, it is suggested that FMPS dietary supplement can be potentially used to intervene UC.

摘要

范围

溃疡性结肠炎(UC)是一种常见的慢性复发性炎症性肠病。本研究试图从肠道微生物与肠道辅助性 T 细胞 17(Th17)/调节性 T 细胞(Treg)平衡的协调相互作用的角度揭示花菇多糖(FMPS)对 UC 的改善机制。

方法和结果

采用葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠模型进行实验。结果表明,FMPS 上调了结肠炎小鼠中紧密连接蛋白 occludin、ZO-1 和 MUC2 的表达,下调了 TNF-α、IL-1β 和 IL-6 的分泌。重要的是,FMPS 恢复了肠道 Th17/Treg 平衡。同时,FMPS 可以调节肠道微生物群,提高结肠炎小鼠中短链脂肪酸(SCFAs)的水平。肠道微生物群耗竭和粪便微生物群移植(FMT)实验表明,FMPS 通过肠道微生物群改善 UC。流式细胞术进一步证明,FMPS 以微生物依赖的方式恢复肠道 Th17/Treg 平衡。

结论

这些结果表明,FMPS 具有改善 UC 的潜力,其机制依赖于肠道微生物介导的 Th17/Treg 平衡的恢复。因此,建议 FMPS 膳食补充剂可潜在用于干预 UC。

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