长非编码RNA NR_030777 通过促进自细胞 - 淋巴细胞融合减轻纳米颗粒诱导的神经退行性损伤
Xinpei Lin1,2, Cheng Chen1,2, Jinxiang Chen1
1Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province 350122, China.
ACS nano
|August 28, 2024
概括
纳米粒子 (CoNPs) 通过损害自而导致神经退行. 长非编码RNANR_030777通过稳定TFEB来保护这种损伤,从而提供了一个潜在的治疗点.
科学领域:
- 环境健康 环境健康
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
背景情况:
- 纳米粒子 (CoNPs) 在工业和医疗应用中越来越普遍.
- 越来越多的证据将CoNP暴露与神经毒性联系在一起,但机制仍然不清楚.
- 需要对CoNP诱导的中枢神经系统 (CNS) 损伤进行系统评估.
研究的目的:
- 在体内和体外研究CoNPs的神经退行性影响.
- 阐明CoNP诱导的神经毒性背后的分子机制,专注于自.
- 探索长非编码RNANR_030777.7的潜在保护作用.
主要方法:
- 在体内和体外模型被用于评估CoNP暴露效应.
- 分析了自细胞形成,溶酶体融合和TFEB水平.
- 研究了NR_030777表达及其与TFEB mRNA的相互作用.
主要成果:
- CoNPs诱导神经退行,认知障碍,β-粉样沉积和Tau过酸化.
- CoNPs通过阻碍自体-溶解体融合和降低TFEB水平来破坏自体流动.
- 过度表达NR_030777通过稳定TFEB mRNA减轻了CoNP诱导的神经毒性.
结论:
- 自功能障碍是CoNP诱导的神经退行的一个关键机制.
- NR_030777通过恢复自-溶酶体功能,对CoNP神经毒性起到保护作用.
- 这项研究提出了CoNP中枢神经系统毒性评估的不良结果途径.
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