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通过CSF-1R/PLCγ2/ERK/Nrf2通路,CuO-NP诱导BV2细胞的亡和功能障碍

Linhui Yang^1,2, Lina Zhu^1,2, Bencheng Lin²

¹College of Oceanography and Ecological Science, Shanghai Ocean University, Shanghai 201306, China.

|April 25, 2025

概括

氧化铜纳米粒子 (CuO-NPs) 通过诱导微质中的氧化应激和炎症引起神经毒性. 这项研究揭示了CuO-NP激活了特定的亡途径,导致神经功能损伤.

科学领域:

神经科学和毒理学是神经科学和毒理学.
纳米材料安全性和生物相互作用

背景情况:

氧化铜纳米粒子 (CuO-NPs) 与神经系统疾病,神经炎症和神经毒性有关.
导致CuO-NP神经毒性的精确机制,包括颗粒大小和铜离子 (Cu2+) 对微质的影响,仍未得到充分研究.

研究的目的:

调查不同颗粒大小的CuO-NP及其相关铜离子在BV2微中的毒性和潜在机制.
阐明CuO-NPs在氧化应激,炎症,亡以及微质中的特定信号通路中的作用.

主要方法:

BV2微质被暴露于小 (S-CuO-NPs) 和大 (L-CuO-NPs) CuO-NPs,等分体Cu2+ (Equ组),以及沉的Cu2+ (Pre组).
分析了细胞活力,形态,细胞亡,氧化应激标志物,炎症反应和关键蛋白质表达 (CSF-1R,PLCγ2,ERK,Nrf2,Bcl-2,Bax,分裂的酶-3,CX3CR1,BDNF,IGF-1).
时间和剂量依赖的毒性评估在12小时和24小时进行.

主要成果:

所有暴露组都表现出细胞活性降低,形态损伤和亡增加,毒性随时间和剂量而升级.
同位体Cu2+组显示出最高的毒性,其次是S-CuO-NPs,L-CuO-NPs和Pre组.
S-CuO-NPs诱导了氧化应激,炎症,增加了膜透性,并激活了CSF-1R/PLCγ2/ERK/Nrf2亡通路,同时降低了神经营养因素的调节.

结论:

通过氧化应激,CuO-NP促进微质中的神经炎症,激活特定的亡途径 (CSF-1R/PLCγ2/ERK/Nrf2).
暴露于CuO-NP会损害微质修复和保护功能,最终导致神经功能损伤.
颗粒大小和铜离子释放显著影响CuO-NP神经毒性.

关键词:

在CSF-1R/PLCγ2/ERK/Nrf2路径中.在CuO-NPs中,它是最重要的.细胞亡是细胞的亡.功能障碍功能障碍功能障碍微质细胞中的微质细胞

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