长期暴露于极低频电磁场对阿尔茨海默病模型大鼠β-淀粉样蛋白沉积和小胶质细胞的影响

A. Komaki, I. Salehi, Arman Keymoradzadeh, Masoumeh Taheri Azandaryani, Zoleikha Golipoor
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引用次数: 0

摘要

背景:近年来,研究人员已将极低频电磁场(ELF-EMFs)作为一种非侵入性治疗方法,用于治疗包括阿尔茨海默病(AD)在内的许多严重神经系统疾病。AD是一种进行性神经退行性疾病,以脑内淀粉样斑块沉积为特征。然而,小胶质细胞的增加增加了吞噬作用和淀粉样斑块的破坏。因此,本研究旨在探讨ELF-EMFs暴露前后AD动物模型中β-淀粉样蛋白前体沉积量和小胶质细胞数量的变化。目的:研究磁波作用前后阿尔茨海默病动物模型β -淀粉样蛋白前体沉积及小胶质细胞数量的变化。方法:50只雄性成年大鼠随机分为5组:对照组、ELF-EMFs组、AD组、治疗组1、治疗组2。研究结束后,处死动物进行免疫组化评估,检测并比较β-淀粉样蛋白沉积和异体移植物炎症因子1 (Iba1)蛋白的产生。结果:ELF降低了β-淀粉样蛋白的沉积,增加了小胶质细胞。然而,这些变化在对照组和elf - emf组之间没有差异(P<0.001)。结论:ELF-EMF可减少β-淀粉样斑块的形成,诱导小胶质细胞的增殖。因此,它们可用于治疗阿尔茨海默病引起的脑损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields on β-amyloid Deposition and Microglia Cells in an Alzheimer Model in Rats
Background: Recently, researchers have considered extremely low-frequency electromagnetic fields (ELF-EMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increases phagocytosis and the destruction of amyloid plaques. Therefore, the present study aimed to investigate the amount of β-amyloid precursor deposition and the number of microglia cells in the animal model of AD before and after exposure to ELF-EMFs. Objective: The aim of this study was to investigate the deposition of beta ameloid precursor and the number of microglial cells in the Alzheimer's animal model before and after exposure to magnetic waves. Methods: Fifty male adult rats were randomly grouped into 5: The control group, the ELF-EMFs group, the AD group, the treatment group 1, and the treatment group 2. After the study period, the animals were killed for immunohistochemistry assessment to detect and compare the deposition of β-amyloid and the production of allograft inflammatory factor 1 (Iba1) protein. Results: Exposure to ELF reduced the deposition of β-amyloid and increased microglia cells. However, these changes were not different between the control and ELF-EMFs groups (P<0.001). Conclusion: ELF-EMF can reduce the formation of β-amyloid plaques and induce the proliferation of microglia cells. Therefore, they can be used to treat brain damage caused by Alzheimer disease.
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