A new intestinal supplement 'Synbiotics' therapeutically regulates gut microbiota and activates PPARs pathway to inhibit Alzheimer's disease progression in mouse models.

IF 1.5 4区 医学 Q4 MICROBIOLOGY New Microbiologica Pub Date : 2024-05-01
Yanan Tong, Guoxiu Lu, Jia Guo, Miao Liu, Yinxing Dai, Jinxin Zhang, Xinru Xu, Zhiguo Wang, Guoxu Zhang
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引用次数: 0

Abstract

We aimed to investigate the role of Synbiotic preparations on the interaction of gut microbiota with AD development. APP/PS1 mice were randomized into APP/PS1 and Synbiotics groups, and C57BL/6J mice were used as wild type (WT) control group. The mice in the Synbiotics group and the APP/PS1 group were given Synbiotics and xylo-oligosaccharides for 3 months, respectively. The mice in the WT group were given the same amount of normal saline. Cognitive function was measured. Positron emission computed tomography/magnetic resonance imaging (PET/MRI) was used to detect fasting blood glucose level. Immunohistochemical assay, ELISA, western blot and qRT-PCR were carried out to detect inflammatory factors. DNA extraction of fecal sample was performed to carry out sequencing. Bioinformatics analysis, metabolites sample preparation and Liquid Chromatograph Mass Spectrometer (LC/MS) analysis were also performed. Synbiotics treatment can significantly ameliorate learning and memory competence by inhibiting Aβ protein deposition. Different bacteria in the intestine were significantly improved and changes in gut microbiota can affect the intestinal metabolism to affect multiple potential pathways after Synbiotics treatment. Synbiotics treatment can activate peroxisome proliferator activated receptor (PPARs) signaling pathway and significantly reduce neuroinflammation in APP/PS1 mice brains. Synbiotics treatment can effectively reduce neuro-inflammatory response through the regulation of intestinal microflora to delay AD development.

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一种新型肠道补充剂 "Synbiotics "能调节肠道微生物群并激活 PPARs 通路,从而抑制小鼠模型中阿尔茨海默病的进展。
我们的目的是研究合成益生菌制剂对肠道微生物群与AD发展之间相互作用的作用。将APP/PS1小鼠随机分为APP/PS1组和益生元组,C57BL/6J小鼠作为野生型(WT)对照组。合成益生菌组和APP/PS1组小鼠分别服用合成益生菌和木寡糖3个月。WT组的小鼠则饮用等量的生理盐水。测量认知功能。正电子发射计算机断层扫描/磁共振成像(PET/MRI)用于检测空腹血糖水平。采用免疫组化、ELISA、Western 印迹和 qRT-PCR 检测炎症因子。对粪便样本进行 DNA 提取以进行测序。此外,还进行了生物信息学分析、代谢物样本制备和液相色谱质谱仪(LC/MS)分析。通过抑制Aβ蛋白沉积,合成益生菌可明显改善学习和记忆能力。肠道中的不同细菌得到明显改善,肠道微生物群的变化会影响肠道代谢,从而影响多种潜在途径。合成益生菌能激活过氧化物酶体增殖激活受体(PPARs)信号通路,明显减轻APP/PS1小鼠大脑神经炎症。合成益生菌治疗可通过调节肠道微生物菌群有效降低神经炎症反应,从而延缓AD的发展。
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来源期刊
New Microbiologica
New Microbiologica 生物-微生物学
CiteScore
2.20
自引率
5.60%
发文量
40
审稿时长
6-12 weeks
期刊介绍: The publication, diffusion and furtherance of research and study on all aspects of basic and clinical Microbiology and related fields are the chief aims of the journal.
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