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凝胶多糖通过肠-脑轴预防高脂饮食诱导的小鼠认知缺陷。

Curdlan Prevents the Cognitive Deficits Induced by a High-Fat Diet in Mice via the Gut-Brain Axis.

作者信息

Yang Xiaoying, Zheng Mingxuan, Hao Shanshan, Shi Hongli, Lin Danhong, Chen Xi, Becvarovski Alec, Pan Wei, Zhang Peng, Hu Minmin, Huang Xu-Feng, Zheng Kuiyang, Yu Yinghua

机构信息

Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogen Biology and Immunology, Xuzhou Medical University, Xuzhou, China.

Illawarra Health and Medical Research Institute (IHMRI), School of Medicine, University of Wollongong, Wollongong, NSW, Australia.

出版信息

Front Neurosci. 2020 May 14;14:384. doi: 10.3389/fnins.2020.00384. eCollection 2020.

DOI:10.3389/fnins.2020.00384
PMID:32477045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7239995/
Abstract

A high-fat (HF) diet is a major predisposing factor of neuroinflammation and cognitive deficits. Recently, changes in the gut microbiota have been associated with neuroinflammation and cognitive impairment, through the gut-brain axis. Curdlan, a bacterial polysaccharide widely used as food additive, has the potential to alter the composition of the microbiota and improve the gut-brain axis. However, the effects of curdlan against HF diet-induced neuroinflammation and cognitive decline have not been investigated. We aimed to evaluate the neuroprotective effect and mechanism of dietary curdlan supplementation against the obesity-associated cognitive decline observed in mice fed a HF diet. C57Bl/6J male mice were fed with either a control, HF, or HF with curdlan supplementation diets for 7 days (acute) or 15 weeks (chronic). We found that acute curdlan supplementation prevented the gut microbial composition shift induced by HF diet. Chronic curdlan supplementation prevented cognitive declines induced by HF diet. In addition, curdlan protected against the HF diet-induced abnormities in colonic permeability, hyperendotoxemia, and colonic inflammation. Furthermore, in the prefrontal cortex (PFC) and hippocampus, curdlan mitigated microgliosis, neuroinflammation, and synaptic impairments induced by a HF diet. Thus, curdlan-as a food additive and prebiotic-can prevent cognitive deficits induced by HF diet via the colon-brain axis.

摘要

高脂(HF)饮食是神经炎症和认知缺陷的主要诱发因素。最近,肠道微生物群的变化已通过肠-脑轴与神经炎症和认知障碍相关联。可德兰(一种广泛用作食品添加剂的细菌多糖)有可能改变微生物群的组成并改善肠-脑轴。然而,可德兰对高脂饮食诱导的神经炎症和认知衰退的影响尚未得到研究。我们旨在评估膳食补充可德兰对高脂饮食喂养小鼠中观察到的肥胖相关认知衰退的神经保护作用及其机制。将C57Bl/6J雄性小鼠分别喂食对照饮食、高脂饮食或添加可德兰的高脂饮食7天(急性)或15周(慢性)。我们发现,急性补充可德兰可防止高脂饮食引起的肠道微生物组成变化。慢性补充可德兰可防止高脂饮食引起的认知衰退。此外,可德兰可预防高脂饮食诱导的结肠通透性异常、高内毒素血症和结肠炎症。此外,在额叶前皮质(PFC)和海马体中,可德兰减轻了高脂饮食诱导的小胶质细胞增生、神经炎症和突触损伤。因此,可德兰作为一种食品添加剂和益生元,可通过结肠-脑轴预防高脂饮食诱导的认知缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/ed174a6c1864/fnins-14-00384-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/39f9bfd70dec/fnins-14-00384-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/ed174a6c1864/fnins-14-00384-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/39f9bfd70dec/fnins-14-00384-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/2a7a84e1042c/fnins-14-00384-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/5ac0b051810e/fnins-14-00384-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/3c54b44b07df/fnins-14-00384-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1215/7239995/ed174a6c1864/fnins-14-00384-g005.jpg

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