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69-2与低聚半乳糖联合通过调节小鼠的AMPK/SIRT1信号通路和肠道微生物群减轻d-半乳糖诱导的衰老。

69-2 Combined with Galacto-Oligosaccharides Alleviates d-Galactose-Induced Aging by Regulating the AMPK/SIRT1 Signaling Pathway and Gut Microbiota in Mice.

作者信息

Wang Wan, Liu Fei, Xu Cong, Liu Zhijing, Ma Jiage, Gu Liya, Jiang Zhanmei, Hou Juncai

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. 2021 Mar 10;69(9):2745-2757. doi: 10.1021/acs.jafc.0c06730. Epub 2021 Feb 10.

Abstract

Probiotics and prebiotics for preventing and alleviating the degenerative changes associated with aging have received extensive attention. In the present work, () 69-2 with the highest antioxidant capacity combined with galacto-oligosaccharide (GOS) was used in aging model mice to evaluate the effect on aging and the regulation of gut microbiota. The combination of 69-2 and GOS supplementation could significantly ( 0.05) improve liver function, antioxidant capacity, and inflammation accompanied by regulating the gut microbiota, increasing the short chain fatty acid (SCFA) levels, and activating the hepatic AMPK/SIRT1 regulatory pathway. The results showed that 69-2 and GOS could activate the hepatic AMPK/SIRT1 signaling pathway by regulating the gut microbiota and metabolites through the liver-gut axis to restore hepatic antioxidant activity to alleviate aging. The study provided a new insight for targeting the gut microbiota to relieve aging through the gut-liver axis.

摘要

用于预防和缓解与衰老相关的退行性变化的益生菌和益生元受到了广泛关注。在本研究中,将具有最高抗氧化能力的()69 - 2与低聚半乳糖(GOS)联合用于衰老模型小鼠,以评估其对衰老的影响以及对肠道微生物群的调节作用。补充69 - 2和GOS的组合可通过调节肠道微生物群、提高短链脂肪酸(SCFA)水平以及激活肝脏AMPK/SIRT1调节途径,显著(P < 0.05)改善肝功能、抗氧化能力和炎症。结果表明,69 - 2和GOS可通过肝脏 - 肠道轴调节肠道微生物群和代谢产物,激活肝脏AMPK/SIRT1信号通路,恢复肝脏抗氧化活性以减轻衰老。该研究为通过肠 - 肝轴靶向肠道微生物群来缓解衰老提供了新的见解。

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