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棉子糖通过重新平衡 Treg/Th17 并激活丁酸盐衍生的 PPARγ 信号通路发挥抗结肠炎作用。

Stachyose Exerts Anticolitis Efficacy by Re-balancing Treg/Th17 and Activating the Butyrate-Derived PPARγ Signaling Pathway.

机构信息

School of Basic Medicine, Qingdao Medical College, Qingdao University, Qingdao 266003, China.

Vinmec-VinUni Institute of Immunology, Vinmec Healthcare System, Hanoi 100000, Vietnam.

出版信息

J Agric Food Chem. 2024 May 29;72(21):12171-12183. doi: 10.1021/acs.jafc.4c01387. Epub 2024 May 15.

Abstract

Ulcerative colitis (UC) is a complex chronic inflammatory disease closely associated with gut homeostasis dysfunction. The previous studies have shown that stachyose, a functional food additive, has the potential to enhance gut health and alleviate UC symptoms. However, the underlying mechanism of its effects remains unknown. In this study, our findings showed that dietary supplements of stachyose had a significant dose-dependent protective effect on colitis symptoms, regulation of gut microbiota, and restoration of the Treg/Th17 cell balance in dextran sulfate sodium (DSS) induced colitis mice. To further validate these findings, we conducted fecal microbiota transplantation (FMT) to treat DSS-induced colitis in mice. The results showed that microbiota from stachyose-treated mice exhibited a superior therapeutic effect against colitis and effectively regulated the Treg/Th17 cell balance in comparison to the control group. Moreover, both stachyose supplementation and FMT resulted in an increase in butyrate production and the activation of PPARγ. However, this effect was partially attenuated by PPARγ antagonist GW9662. These results suggested that stachyose alleviates UC symptoms by modulating gut microbiota and activating PPARγ. In conclusion, our work offers new insights into the benefical effects of stachyose on UC and its potential role in modulating gut microbiota.

摘要

溃疡性结肠炎(UC)是一种复杂的慢性炎症性疾病,与肠道稳态功能障碍密切相关。先前的研究表明,作为一种功能性食品添加剂,棉子糖具有增强肠道健康和缓解 UC 症状的潜力。然而,其作用的潜在机制尚不清楚。在这项研究中,我们的研究结果表明,棉子糖的膳食补充剂对葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠的结肠炎症状、肠道微生物群的调节以及 Treg/Th17 细胞平衡的恢复具有显著的剂量依赖性保护作用。为了进一步验证这些发现,我们进行了粪便微生物群移植(FMT)来治疗 DSS 诱导的结肠炎小鼠。结果表明,与对照组相比,来自棉子糖处理组的微生物群对结肠炎具有更好的治疗效果,有效地调节了 Treg/Th17 细胞平衡。此外,棉子糖补充和 FMT 均导致丁酸产生增加和 PPARγ 激活。然而,PPARγ 拮抗剂 GW9662 部分减弱了这种作用。这些结果表明,棉子糖通过调节肠道微生物群和激活 PPARγ 来缓解 UC 症状。总之,我们的工作为棉子糖对 UC 的有益作用及其在调节肠道微生物群中的潜在作用提供了新的见解。

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