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来自服用桑椹(桑科植物桑Morus alba L.)多酚和多糖的小鼠的肠道微生物群激活PPARα/PGC-1α信号通路,以减轻高脂饮食诱导的小鼠代谢综合征。

Gut microbiota from Mori fructus (Morus alba L.) polyphenols and polysaccharides-dosed mice activates the PPARα/PGC-1α signaling pathway to mitigate HFD-induced metabolic syndrome in mice.

作者信息

Wan Meixia, Li Qing, Xiao Yudie, Zhou Dan, Lei Qianya, Wang Shu

机构信息

Medicine School, Longdong University, Qingyang, 745000, China.

West China School of Pharmacy, Sichuan University, Chengdu, 610041, China.

出版信息

Sci Rep. 2025 Aug 1;15(1):28137. doi: 10.1038/s41598-025-13715-8.


DOI:10.1038/s41598-025-13715-8
PMID:40750814
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12316889/
Abstract

Mori Fructus, rich in polysaccharides and polyphenols, has long been used in East Asia as a functional food and medicinal agent. In traditional Chinese medicine, it is used to treat various ailments like wasting-thirst syndrome and constipation. Studies suggest its extract fractions may alleviate metabolic syndrome symptoms by affecting gut microbiota. To explore this, fecal microbiota transplantation (FMT) was used in an experiment. Pseudo-germ-free mice were created with antibiotics and given a high-fat, high-sugar diet (HFD) to induce metabolic syndrome. Then, fecal bacterial infusions were transplanted. Results showed significant improvement in metabolic syndrome parameters in the FMT-MFPS(fecal microbiota transplantation-Mori Fructus polyphenols plus polysaccharides) group. Dyslipidemia, liver, and kidney injuries were modulated in treated mice. The PPARα/PGC-1α signaling pathway was activated. These findings indicate Mori Fructus extract fractions prevent metabolic syndrome via gut microbiota modulation, with effects sustained through FMT, providing a reference for prevention.

摘要

桑椹富含多糖和多酚,长期以来在东亚地区被用作功能性食品和药物。在传统中医中,它被用于治疗各种疾病,如消渴症和便秘。研究表明,其提取物组分可能通过影响肠道微生物群来缓解代谢综合征症状。为了探究这一点,在一项实验中使用了粪便微生物群移植(FMT)。用抗生素创建伪无菌小鼠,并给予高脂高糖饮食(HFD)以诱导代谢综合征。然后,进行粪便细菌输注移植。结果显示,FMT-MFPS(粪便微生物群移植-桑椹多酚加多糖)组的代谢综合征参数有显著改善。治疗小鼠的血脂异常、肝脏和肾脏损伤得到调节。PPARα/PGC-1α信号通路被激活。这些发现表明,桑椹提取物组分通过调节肠道微生物群预防代谢综合征,其效果通过FMT得以持续,为预防提供了参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/008f0dca203f/41598_2025_13715_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/a0301b9e596f/41598_2025_13715_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/e7ae5860ea91/41598_2025_13715_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/576655d846dc/41598_2025_13715_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/1bfac561d931/41598_2025_13715_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/ef6b2400caef/41598_2025_13715_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/008f0dca203f/41598_2025_13715_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/a0301b9e596f/41598_2025_13715_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/e7ae5860ea91/41598_2025_13715_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/576655d846dc/41598_2025_13715_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/1bfac561d931/41598_2025_13715_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/ef6b2400caef/41598_2025_13715_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a92f/12316889/008f0dca203f/41598_2025_13715_Fig6_HTML.jpg

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本文引用的文献

[1]
LZys1 modulates gut microbiota, diminishes ileal FXR-FGF15 signaling, and regulates hepatic function.

Microbiol Spectr. 2025-6-3

[2]
New insights into the interplay between autophagy, gut microbiota and insulin resistance in metabolic syndrome.

Biomed Pharmacother. 2024-7

[3]
Carboxymethylated Abrus cantoniensis polysaccharide prevents CTX-induced immunosuppression and intestinal damage by regulating intestinal flora and butyric acid content.

Int J Biol Macromol. 2024-3

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Biomedicines. 2023-12-22

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Nutrients. 2023-12-29

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Gut Microbes. 2023-12

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Nature. 2023-9

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Nutrients. 2023-5-5

[9]
Dietary Supplementation with Epicatechin Improves Intestinal Barrier Integrity in Mice.

Foods. 2022-10-21

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Cell Host Microbe. 2023-5-10

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