Wu Qiong, Li Qifa, Zhang Xuan, Ntim Michael, Wu Xuefei, Li Ming, Wang Li, Zhao Jie, Li Shao
Liaoning Provincial Key Laboratory of Cerebral Diseases in Department of Physiology, Dalian Medical University, Dalian, China.
Functional Laboratory, Dalian Medical University, Dalian, China.
PeerJ. 2020 Oct 28;8:e10262. doi: 10.7717/peerj.10262. eCollection 2020.
Alzheimer's disease (AD), being a complex disorder, is affected either by genetic or environmental factors or both. It is observed that there is an excessive accumulation of amyloid β (Aβ) in the extracellular space of the brain. AD is the first neurodegenerative disease in the elderly, and so far there is no effective treatment. In recent years, many studies have reported that Alzheimer's disease has a relationship with gut microflora, indicating that regulating gut microbiota could offer therapeutic intervention for AD. This study explored the effect has in averting AD.
WT and APP/PS1 mice were used for the experiments. The mice were randomly assigned to four groups: WT group, WT + Bi group, AD group (APP/PS1 mouse) and AD + Bi group (treated APP/PS1 mouse). Treatment with lasted for 6 months and mice were prepared for immunohistochemistry, immunofluorescence, Thioflavin S staining, Western blotting, PCR and Elisa quantitative assay.
The results show that after 6 months of treatment with signiis to be lesficantly reduces Aβ deposition in cortex and hippocampus of AD mice. The level of insoluble Aβ in the hippocampus and cortex of AD+Bi mice was decreased compared with AD mice. Meanwhile, a significant decrease in the level of soluble Aβ in the cortex of AD+Bi mice but not in the hippocampus was observed. The activation of microglia and the release of inflammatory factors were also determined in this study. From the results, inhibited microglial activation and reduced IL-1β, TNF-α, IL-4, IL-6 and INF-γ release. Altogether, these results implied that can alleviate the pathological changes of AD through various effects.
阿尔茨海默病（AD）是一种复杂的疾病，受遗传或环境因素或两者共同影响。据观察，大脑细胞外空间中淀粉样β蛋白（Aβ）过度积累。AD是老年人中第一种神经退行性疾病，迄今为止尚无有效治疗方法。近年来，许多研究报告称阿尔茨海默病与肠道微生物群有关，这表明调节肠道微生物群可为AD提供治疗干预。本研究探讨了[具体物质]在预防AD方面的作用。
使用野生型（WT）和APP/PS1小鼠进行实验。将小鼠随机分为四组：WT组、WT + [具体物质]组、AD组（APP/PS1小鼠）和AD + [具体物质]组（经治疗的APP/PS1小鼠）。用[具体物质]治疗持续6个月，并对小鼠进行免疫组织化学、免疫荧光、硫黄素S染色、蛋白质印迹、聚合酶链反应（PCR）和酶联免疫吸附测定（ELISA）定量分析。
结果表明，用[具体物质]治疗6个月后，显著降低了AD小鼠皮质和海马中的Aβ沉积。与AD小鼠相比，AD + [具体物质]小鼠海马和皮质中不溶性Aβ水平降低。同时，观察到AD + [具体物质]小鼠皮质中可溶性Aβ水平显著降低，但海马中未降低。本研究还测定了小胶质细胞的激活和炎症因子的释放。结果显示，[具体物质]抑制了小胶质细胞的激活，并减少了白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）、白细胞介素-4（IL-4）、白细胞介素-6（IL-6）和干扰素-γ（INF-γ）的释放。总之，这些结果表明[具体物质]可通过多种作用减轻AD的病理变化。
