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益生元粗多糖与 GG 联合延缓小鼠衰老相关氧化应激。

Prebiotic crude polysaccharides combined with GG postpone aging-related oxidative stress in mice.

机构信息

College of Food Science, Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, China.

School of Medicine, South China University of Technology, Guangzhou, Guangdong 510006, China.

出版信息

Food Funct. 2022 Feb 7;13(3):1218-1231. doi: 10.1039/d1fo02079j.

Abstract

This study aimed to investigate the potential anti-aging mechanisms of crude polysaccharides (APS), when used synergistically with GG (APS + LGG) in a D-galactose-induced aging mouse model. In the Morris water maze test, APS + LGG showed a significantly higher memory and learning capacity compared to untreated, APS only treated and LGG treated mice. This was thought to be mediated by increased levels of brain-derived neurotrophic factor, which decreased escape latency. In addition to this, in the aging mouse model, APS + LGG co-treatment markedly alleviated liver oxidation and metabolism by enhancing the antioxidant activity of enzymes; this decreased the lipid metabolism and peroxidation levels. Furthermore, high throughput sequencing analysis revealed that an APS + LGG supplemented feed increased the relative abundance of positive bacteria in the gut microbiota such as and . Importantly, and showed a negative relationship with low density lipoprotein-cholesterol in the Spearman correlation analysis. These results illustrate that APS, in combination with LGG, postponed aging related oxidative stress when used as a prebiotic. The proposed mechanism for this is the reduction in liver oxidation and lipid metabolism, as well as the regulation of gut microbiota.

摘要

本研究旨在探讨粗多糖(APS)与长双歧杆菌(LGG)协同作用(APS+LGG)对 D-半乳糖诱导衰老模型小鼠的潜在抗衰老机制。在 Morris 水迷宫试验中,与未处理组、仅 APS 处理组和仅 LGG 处理组相比,APS+LGG 表现出更高的记忆和学习能力。这被认为是通过增加脑源性神经营养因子的水平来介导的,从而降低了逃避潜伏期。此外,在衰老小鼠模型中,APS+LGG 共同处理通过增强抗氧化酶的活性显著减轻了肝脏氧化和代谢,从而降低了脂质代谢和过氧化水平。此外,高通量测序分析表明,APS+LGG 补充饲料增加了肠道微生物群中阳性菌的相对丰度,如 和 。重要的是,Spearman 相关性分析显示, 和 与低密度脂蛋白胆固醇呈负相关。这些结果表明,APS 与 LGG 联合使用作为一种益生元可以延缓与氧化应激相关的衰老。提出的机制是降低肝脏氧化和脂质代谢,以及调节肠道微生物群。

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