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苹果多糖通过微生物群-肠-脑轴改善年龄匹配的认知障碍和肠道衰老。

Apple polysaccharide improves age-matched cognitive impairment and intestinal aging through microbiota-gut-brain axis.

机构信息

Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Nanchang University, 330000, Nanchang, Jiangxi, People's Republic of China.

The Institute of Translational Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, People's Republic of China.

出版信息

Sci Rep. 2024 Jul 13;14(1):16215. doi: 10.1038/s41598-024-67132-4.

Abstract

The Apple polysaccharides (AP), extracted from the fruit of apple, has been used to treat multiple pathological diseases. In this study, we evaluated the effects of AP on cognitive impairment and intestinal aging in naturally aging mice. As a result, it was found that AP could improve spatial learning and memory impairment in aging mice through the Morris water maze experiment. Additionally, AP intervention can upregulate the expression of nerve growth factor (BDNF), postsynaptic marker (PSD95), and presynaptic marker (SYP) proteins. Moreover, AP can enhance total antioxidant capacity, reduce the level of pro-inflammatory cytokine, and inhibit the activation of the NF-κB signaling pathway, exerting anti-inflammatory and antioxidant functions. And the administration of AP restored intestinal mucosal barrier function, reduced the expression of aging and apoptosis related proteins. The administration of AP also altered the gut microbiota of mice. At the genus level, AP decreased the abundance of Helicobacter and Bilophila, while increased the abundance of Lactobacillus and Bacteroides. In summary, these data demonstrate that AP treatment can alleviate cognitive impairment, oxidative stress, and inflammatory reactions, repair the intestinal mucosal barrier, reduce intestinal aging, and alter specific microbial characteristics, ultimately improving the health of the elderly.

摘要

苹果多糖(AP)是从苹果果实中提取的,已被用于治疗多种病理疾病。在这项研究中,我们评估了 AP 对自然衰老小鼠认知障碍和肠道衰老的影响。结果发现,AP 通过 Morris 水迷宫实验可以改善衰老小鼠的空间学习和记忆障碍。此外,AP 干预可以上调神经生长因子(BDNF)、突触后标志物(PSD95)和突触前标志物(SYP)蛋白的表达。此外,AP 可以增强总抗氧化能力,降低促炎细胞因子水平,并抑制 NF-κB 信号通路的激活,发挥抗炎和抗氧化作用。AP 的给药恢复了肠道黏膜屏障功能,降低了与衰老和细胞凋亡相关蛋白的表达。AP 的给药还改变了小鼠的肠道微生物群。在属水平上,AP 降低了 Helicobacter 和 Bilophila 的丰度,而增加了 Lactobacillus 和 Bacteroides 的丰度。总之,这些数据表明 AP 治疗可以减轻认知障碍、氧化应激和炎症反应,修复肠道黏膜屏障,减少肠道衰老,并改变特定的微生物特征,最终改善老年人的健康状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a01/11246462/0626f43a26c6/41598_2024_67132_Fig1_HTML.jpg

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