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