氨基基改性聚乙烯纳米塑料诱导内皮皮质亡和亲静脉细胞反应
Junliang Chen1, Ye Cheng1, Jining Wang1
1Department of Biological Sciences, School of life Science, Liaoning University, Chongshan Road 66, Shenyang 110036, P.R. China.
概括
微小的纳米塑料 (NP),特别是氨基基基改性NP (NH2-NP),可以通过触发细胞死亡途径来损害血管. 这项研究揭示了这些NP如何影响内皮细胞和免疫细胞,影响心血管健康.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 纳米塑料 (NP) 对人类健康,特别是心血管系统构成越来越大的威胁.
- NP诱导的血管损伤的精确细胞机制在很大程度上是未知的.
- 表面的修改,如氨基群 (NH2-NP),显著改变NP的毒性.
研究的目的:
- 研究NP大小和氨基基基修饰对人类静脉内皮细胞 (HUVECs) 的影响.
- 阐明纳米塑料诱导的血管损伤背后的细胞机制.
- 评估灭菌在纳米塑料毒性的作用.
主要方法:
- 对HUVEC暴露于各种尺寸的纳米塑料,包括氨基基改性NP (NH2-NP).
- 分析与热致死相关的蛋白质表达和细胞活性的分析.
- 在NP暴露后评估THP-1细胞的招募,粘附,迁移和脂质积累.
- 利用热致死抑制剂VX-765来确认途径的参与.
主要成果:
- 20nm的NH2-NPs在HUVEC中显著改变了与热死相关的蛋白质表达.
- 通过NF-κB/NLRP3/GSDMD介导的烧途径,NH2-NPs诱导HUVECs损伤.
- NP诱导的HUVECs损伤促进了THP-1细胞粘附,迁移和脂质积累,导致泡细胞的形成.
结论:
- 热致死在NH2-NP诱导的内皮细胞损伤中发挥着关键作用.
- 表面化学修饰,如氨基功能化,对于确定NP血管毒性至关重要.
- 这些发现为纳米塑料的血管毒性及其对免疫细胞行为的影响提供了洞察力.
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