来自人间充质干细胞的胶质样细胞通过减少NLRP-3炎性体保护阿尔茨海默病体外模型中的神经干细胞

Dementia and neurocognitive disorders Pub Date : 2021-01-01 Epub Date: 2020-11-27 DOI:10.12779/dnd.2021.20.1.1
Mina Hwang, Se Hyeon Song, Mi-Sook Chang, Seong-Ho Koh
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引用次数: 2

摘要

背景与目的:神经干细胞(Neural stem cells, NSCs)具有再生、增殖和分化的能力,在受损神经系统的修复中发挥着重要作用。然而,在阿尔茨海默病(AD)等神经退行性疾病中,NSCs也会受损。来自人间充质干细胞(ghMSCs)的胶质样细胞是功能增强的成体干细胞。在本研究中,我们研究了ghMSCs是否可以保护NSCs免受β淀粉样蛋白(Aβ)介导的毒性。方法:从E13-14胎鼠皮质提取大鼠神经干细胞。将NSCs接种于预包被板中,第二天,细胞同时接受20 μM Aβ和0.4 μM孔插入的种子良好的ghMSCs处理。共处理48h后,观察细胞活力和增殖情况。共治疗2小时后,采用western blotting检测炎症小体相关因子,如nod样受体家族pyrin domain containing 3、caspase-1和白细胞介素-1β。结果:结果显示,ghMSCs通过降低Aβ诱导的NSCs NRLP3炎性体的激活,提高了Aβ损伤NSCs的活力和增殖,降低了其毒性。结论:在本研究中,我们证实了ghMSCs可以通过调节炎症反应来保护AD体外模型中的NSCs。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Glia-Like Cells from Human Mesenchymal Stem Cells Protect Neural Stem Cells in an <i>In Vitro</i> Model of Alzheimer's Disease by Reducing NLRP-3 Inflammasome.

Glia-Like Cells from Human Mesenchymal Stem Cells Protect Neural Stem Cells in an <i>In Vitro</i> Model of Alzheimer's Disease by Reducing NLRP-3 Inflammasome.

Glia-Like Cells from Human Mesenchymal Stem Cells Protect Neural Stem Cells in an In Vitro Model of Alzheimer's Disease by Reducing NLRP-3 Inflammasome.

Background and purpose: Neural stem cells (NSCs) have the ability to regenerate, proliferate, and differentiate, enabling them to play important roles in the recovery of the damaged nervous system. However, in neurodegenerative diseases such as Alzheimer's disease (AD), the NSCs are damaged as well. Glia-like cells from human mesenchymal stem cells (ghMSCs) are functionally enhanced adult stem cells. In the present study, we investigated whether ghMSCs could protect NSCs from amyloid beta (Aβ)-mediated toxicity.

Methods: Rat NSCs were obtained from E13-14 fetal rat cortices. NSCs were seeded in pre-coated plates, and the next day, cells were simultaneously treated with 20 μM Aβ and 0.4 μm pore insert well-seeded ghMSCs. After 48 hours of co-treatment, cell viability and proliferation were evaluated. After 2 hours of co-treatment, western blotting was performed to measure inflammasome-related factors, such as NOD-like receptor family pyrin domain containing 3, caspase-1, and interleukin-1β.

Results: The results showed that ghMSCs increased viability and proliferation and reduced the toxicity of NSCs injured by Aβ by reducing the NRLP3 inflammasome activation of NSCs induced by Aβ.

Conclusions: In this study, we confirmed that ghMSCs could protect NSCs in an in vitro model of AD through the regulation of inflammatory response.

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