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芜菁多糖通过调节微生物群减轻低压缺氧诱导的氧化和肠道损伤。

Brassica rapa L. polysaccharide mitigates hypobaric hypoxia-induced oxidation and intestinal damage via microbiome modulation.

作者信息

Liu Wei, Liu Zhenjiang, Fan Xueni, Li Diantong, Zhao Tingting, Niu Yuanlin, Baima Yangjin, Wen Dongxu, Li Bin, Huang Xiaodan

机构信息

School of Public Health, Lanzhou University, Lanzhou, 730000, China.

Institute of Animal Husbandry and Veterinary Science, Xizang Autonomous Region Academy of Agricultural and Animal Husbandry Sciences, Key Laboratory of Animal Genetics and Breeding on Tibetan Plateau, Ministry of Agriculture and Rural Affairs, Lhasa, 850000, China.

出版信息

NPJ Sci Food. 2024 Dec 27;8(1):112. doi: 10.1038/s41538-024-00365-9.

Abstract

The high-altitude, low-pressure, and hypoxia environment poses a significant threat to human health, particularly causing intestinal damage and disrupting gut microbiota. This study investigates the protective effects of Brassica rapa L. crude polysaccharides (BRP) on intestinal damage in mice exposed to hypobaric hypoxic conditions. Results showed that oxidative stress and inflammation levels were elevated in the hypoxia group, while BRP intervention significantly increased antioxidant enzyme activities (SOD, GSH-Px, T-AOC) and reduced inflammatory markers (IL-6, IL-1β, TNF-α). BRP also restored intestinal barrier function by enhancing claudin-1, occludin, and ZO-1 expression. Notably Chromatographic and metagenomic analyses revealed that BRP enriched butyrate levels, promoted beneficial bacteria like Akkermansia muciniphila and Leuconostoc lactis, and upregulated L-arginine biosynthesis II and L-methionine biosynthesis III pathways to enhance antioxidant activity. Fecal microbiota transfer experiments confirmed the role of gut microbiota in mediating BRP's protective effects, providing valuable insights into prebiotic-based therapeutic strategies for hypobaric hypoxia-induced intestinal damage.

摘要

高海拔、低压和缺氧环境对人类健康构成重大威胁,尤其会导致肠道损伤并破坏肠道微生物群。本研究调查了芜菁粗多糖(BRP)对低压缺氧条件下小鼠肠道损伤的保护作用。结果表明,缺氧组的氧化应激和炎症水平升高,而BRP干预显著提高了抗氧化酶活性(超氧化物歧化酶、谷胱甘肽过氧化物酶、总抗氧化能力),并降低了炎症标志物(白细胞介素-6、白细胞介素-1β、肿瘤坏死因子-α)。BRP还通过增强闭合蛋白-1、闭锁蛋白和紧密连接蛋白-1的表达来恢复肠道屏障功能。值得注意的是,色谱和宏基因组分析表明,BRP提高了丁酸盐水平,促进了嗜黏蛋白阿克曼氏菌和乳酸明串珠菌等有益菌的生长,并上调了L-精氨酸生物合成II和L-蛋氨酸生物合成III途径以增强抗氧化活性。粪便微生物群移植实验证实了肠道微生物群在介导BRP保护作用中的作用,为基于益生元的低压缺氧诱导肠道损伤治疗策略提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2936/11680955/f52f00422415/41538_2024_365_Fig1_HTML.jpg

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