免疫和硫黄素s -染色法评价静脉注射人脂肪源性干细胞后大鼠阿尔茨海默病模型海马中a β沉积

Thrita Pub Date : 2019-01-21 DOI:10.5812/THRITA.88367
Maryam Doshmanziari, A. Sarveazad, F. Moradi, Marjan Shariatpanahi, E. Doshmanziari, S. Simorgh, M. Eftekharzadeh
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引用次数: 3

摘要

背景:阿尔茨海默病(AD)是一种进行性神经精神疾病,逐渐损害记忆和行为功能。淀粉样蛋白(Aβ)被认为是AD患者大脑中毒性最大的物质。目的:本研究旨在评估静脉注射人脂肪源性干细胞(hADSCs)后大鼠AD模型海马中免疫和硫黄素s染色的a β沉积。方法:将32只雄性大鼠分为对照组、假手术组、AD组和hADSCs组。流式细胞术证实了hascs的特征。采用免疫和硫黄素s染色法检测注射hADSCs后大鼠AD模型海马内的a β斑块。结果:统计分析显示,AD组与对照组和假手术组相比,Aβ斑块明显增加。在AD组中,给药hascs可显著降低免疫反应性和硫代s阳性斑块。我们还发现,抗a β抗体(免疫组化染色)检测到的斑块明显多于硫黄素- s检测到的斑块。结论:结果表明,hascs在AD模型大鼠海马迁移后可有效降低淀粉样蛋白聚集。
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Evaluation of Aβ Deposits in the Hippocampus of a Rat Model of Alzheimer’s Disease After Intravenous Injection of Human Adipose Derived Stem Cells by Immuno- and Thioflavin S-Costaining
Background: Alzheimer's disease (AD) is a progressive neuropsychiatric disorder that gradually impairs memory and behavioral functions. Amyloid beta (Aβ) is considered as the most toxic substance in the brain of AD patients. Objectives: The present study was designed to evaluate Aβ deposits by Immuno- and Thioflavin S-costaining in the hippocampus of a rat model of AD after intravenous injection of human adipose-derived stem cells (hADSCs). Methods: Thirty-two male rats were included in the four groups of control, sham, AD and hADSCs. The hADSCs characterization was confirmed by the flow cytometry technique. Immuno- and Thioflavin S-costaining was utilized for detecting Aβ plaques in the hippocampus of a rat model of AD following injection of hADSCs. Results: Statistical analysis revealed that Aβ plaques increased significantly in the AD group compared to the control and sham groups. The administration of hADSCs significantly decreased immunoreactivity and Thio-S-positive plaques in the AD group. We also found that the plaques detected by anti-Aβ antibody (immunohistochemical staining) were significantly more than those distinguished by Thioflavin-S in all the groups. Conclusions: Results showed that hADSCs played an effective role in decreasing amyloids aggregation following migration to the hippocampus of the rat model of AD.
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