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岩藻依聚糖通过保护肠道屏障、抑制丝裂原活化蛋白激酶/核因子-κB通路以及调节肠道微生物群和代谢产物,缓解了因纤维缺乏而加重的结肠炎。

Fucoidan alleviated colitis aggravated by fiber deficiency through protecting the gut barrier, suppressing the MAPK/NF-κB pathway, and modulating gut microbiota and metabolites.

作者信息

Zheng Weiyun, Tang Shuangru, Ren Xiaomeng, Song Shuang, Ai Chunqing

机构信息

School of Agronomy and Life Science, Shanxi Datong University, Datong, China.

National Engineering Research Center of Seafood, School of Food Science and Technology, Dalian Polytechnic University, Dalian, China.

出版信息

Front Nutr. 2025 Jan 24;11:1462584. doi: 10.3389/fnut.2024.1462584. eCollection 2024.

DOI:10.3389/fnut.2024.1462584
PMID:39925971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11802440/
Abstract

Insufficient dietary fiber intake has become a global public health issue, affecting the development and management of various diseases, including intestinal diseases and obesity. This study showed that dietary fiber deficiency enhanced the susceptibility of mice to colitis, which could be attributed to the disruption of the gut barrier integrity, activation of the NF-κB pathway, and oxidative stress. fucoidan (UPF) alleviated colitis symptoms in mice that fed with a fiber deficient diet (FD), characterized by increased weight gain and reduced disease activity index, liver and spleen indexes, and histological score. The protective effect of UPF against FD-exacerbated colitis can be attributed to the alleviation of oxidative stress, the preservation of the gut barrier integrity, and inhibition of the MAPK/NF-κB pathway. UPF ameliorated the gut microbiota composition, leading to increased microbiota richness, as well as increased levels of , , and and reduced levels of , , and . Metabolomics analysis revealed that UPF improved the profile of microbiota metabolites, with increased levels of carnitine and taurine and decreased levels of tyrosine and deoxycholic acid. This study suggests that UPF has the potential to be developed as a novel prebiotic agent to enhance human health.

摘要

膳食纤维摄入不足已成为一个全球性的公共卫生问题,影响着包括肠道疾病和肥胖症在内的各种疾病的发生发展及管理。本研究表明,膳食纤维缺乏会增强小鼠对结肠炎的易感性,这可能归因于肠道屏障完整性的破坏、NF-κB通路的激活以及氧化应激。岩藻依聚糖(UPF)减轻了喂食低纤维饮食(FD)小鼠的结肠炎症状,其特征为体重增加、疾病活动指数、肝脏和脾脏指数以及组织学评分降低。UPF对FD加剧的结肠炎的保护作用可归因于氧化应激的减轻、肠道屏障完整性的维持以及MAPK/NF-κB通路的抑制。UPF改善了肠道微生物群组成,导致微生物群丰富度增加,以及 、 和 水平升高, 、 和 水平降低。代谢组学分析表明,UPF改善了微生物群代谢产物谱,肉碱和牛磺酸水平升高,酪氨酸和脱氧胆酸水平降低。本研究表明,UPF有潜力被开发成为一种新型益生元制剂,以促进人类健康。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/75aef9190a82/fnut-11-1462584-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/83db389ae281/fnut-11-1462584-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/cfc5a973da24/fnut-11-1462584-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/9e457677aa26/fnut-11-1462584-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/4261437ebba1/fnut-11-1462584-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/75aef9190a82/fnut-11-1462584-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/83db389ae281/fnut-11-1462584-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/33c0e38b4989/fnut-11-1462584-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/7d06e3d698d8/fnut-11-1462584-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/15e1a20b7e64/fnut-11-1462584-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/cfc5a973da24/fnut-11-1462584-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/9e457677aa26/fnut-11-1462584-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/4261437ebba1/fnut-11-1462584-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73db/11802440/75aef9190a82/fnut-11-1462584-g009.jpg

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Oral Fucoidan Administration Exhibits Anti-Inflammatory and Antioxidant Properties and Improves DSS-Induced Colitis in C57BL/6J Mice.
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Pharmaceutics. 2022 Nov 4;14(11):2383. doi: 10.3390/pharmaceutics14112383.
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Research Progress on the Protective Effect of Brown Algae-Derived Polysaccharides on Metabolic Diseases and Intestinal Barrier Injury.褐藻源多糖对代谢性疾病及肠道屏障损伤的保护作用研究进展。
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