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灵芝多糖对D-半乳糖致衰老小鼠学习记忆障碍及肠道菌群的影响

Effects of Ganoderma lucidum polysaccharide on learning and memory impairment and intestinal flora in mice with D-galactose-induced aging.

作者信息

Chen Yuyang, Li Jiahui, Zhang Shuang, Zhao Yuehan, Gao Demeng, Xu Guangyu

机构信息

Beihua University, 3999 Binjiang East Road, Jilin, Jilin, 132013, China.

出版信息

Naturwissenschaften. 2025 Jun 2;112(3):46. doi: 10.1007/s00114-025-01997-x.

Abstract

Learning and memory impairment is one of the main manifestations of cognitive impairment. Gut flora can affect cognitive function and behavior through the gut-brain axis. Ganoderma lucidum polysaccharide (GLP) is one of the main effective components of G. lucidum, with antioxidant and anti-aging effects. In this study, the learning and memory impairment model of aging mice was established by injecting D-galactose (D-gal). The learning and memory ability of mice was tested by a water maze experiment. Also, the biochemical indexes of mouse serum and brain tissue were determined. In addition, 16S rRNA sequencing was performed on mouse feces. The results showed that GLP significantly shortened the latency of mice to find a safe platform. Also, they enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, increased glutamate (Glu) and acetylcholine (ACh) contents, and decreased malondialdehyde (MDA) and gamma-aminobutyric acid (GABA) contents in mice to improve antioxidant capacity, remove free radicals, and reduce lipid peroxidation and oxidative stress, thereby improving learning and memory disorders in mice. The analysis of the microflora after the intervention of GLP to improve learning and memory disorders in mice revealed changes in Lactobacillus abundance. In conclusion, D-gal causes learning memory impairment and reduced intestinal microbial diversity in aging mice, whereas GLP may ameliorate learning memory impairment by altering the distribution of Lactobacillus in the intestinal tract of mice and regulating the biosynthesis of peptidoglycan and secondary bile acids.

摘要

学习和记忆障碍是认知障碍的主要表现之一。肠道菌群可通过肠-脑轴影响认知功能和行为。灵芝多糖(GLP)是灵芝的主要有效成分之一,具有抗氧化和抗衰老作用。本研究通过注射D-半乳糖(D-gal)建立衰老小鼠学习和记忆障碍模型,采用水迷宫实验检测小鼠的学习和记忆能力,同时测定小鼠血清和脑组织的生化指标,并对小鼠粪便进行16S rRNA测序。结果显示,GLP显著缩短小鼠找到安全平台的潜伏期,增强超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,增加小鼠体内谷氨酸(Glu)和乙酰胆碱(ACh)含量,降低丙二醛(MDA)和γ-氨基丁酸(GABA)含量,以提高抗氧化能力、清除自由基、减少脂质过氧化和氧化应激,从而改善小鼠的学习和记忆障碍。对GLP干预改善小鼠学习记忆障碍后的微生物群分析显示,乳酸杆菌丰度发生了变化。综上所述,D-gal导致衰老小鼠学习记忆障碍并降低肠道微生物多样性,而GLP可能通过改变小鼠肠道中乳酸杆菌的分布以及调节肽聚糖和次级胆汁酸的生物合成来改善学习记忆障碍。

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