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联合半乳糖寡糖补充剂:通过调节短链脂肪酸和 c-Jun N-末端激酶信号通路来预防神经退行性变和记忆损伤的神经保护方案。

Combined with Galactooligosaccharides Supplement: A Neuroprotective Regimen Against Neurodegeneration and Memory Impairment by Regulating Short-Chain Fatty Acids and the c-Jun N-Terminal Kinase Signaling Pathway in Mice.

机构信息

College of Food Science, Northeast Agricultural University, Harbin, 150030, China.

Key Laboratory of Dairy Science, Ministry of Education, College of Food Science, Northeast Agricultural University, Harbin, 150030, China.

出版信息

J Agric Food Chem. 2022 Jul 20;70(28):8619-8630. doi: 10.1021/acs.jafc.2c01950. Epub 2022 Jul 11.

Abstract

Probiotics and prebiotics have received attention in alleviating neurodegenerative diseases. () 69-2 was combined with galactooligosaccharides (GOS) and supplemented in a d-galactose (d-gal)-induced neurodegeneration and memory impairment mice model to explore its effects on the brain and the regulation of short-chain fatty acids. The results showed that the -GOS supplementation inhibited d-gal-induced oxidative stress and increased the brain's nuclear factor erythroid 2-related factor 2 (Nrf2) levels. Butyrate, a metabolite of the gut microbiota regulated by combined with GOS, inhibits p-JNK expression, downregulates pro-apoptotic proteins expression and the activation of inflammatory mediators, and upregulates synaptic protein expression. This might be a potential mechanism for 69-2 combined with GOS supplementation to alleviate d-gal-induced neurodegeneration and memory impairment. This study sheds new light on the development of aging-related neuroprotective dietary supplements based on the gut-brain axis.

摘要

益生菌和益生元在缓解神经退行性疾病方面受到了关注。()69-2 与半乳糖低聚糖(GOS)结合,并在半乳糖(d-gal)诱导的神经退行性变和记忆障碍小鼠模型中补充,以探索其对大脑的影响和短链脂肪酸的调节。结果表明,GOS 补充抑制了 d-gal 诱导的氧化应激,并增加了大脑的核因子红细胞 2 相关因子 2(Nrf2)水平。由与 GOS 结合调节的肠道微生物群的代谢物丁酸盐,抑制 p-JNK 的表达,下调促凋亡蛋白的表达和炎症介质的激活,并上调突触蛋白的表达。这可能是 69-2 与 GOS 补充联合缓解 d-gal 诱导的神经退行性变和记忆障碍的潜在机制。本研究为基于肠-脑轴的与衰老相关的神经保护膳食补充剂的开发提供了新的思路。

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