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碳核作为环境颗粒物的替代物,通过炎症酶激活诱导血管内皮炎症

Yán Wāng¹, Chunzhi Wang², Yang Jiang²

¹Key laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, China; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China.

Journal of hazardous materials

|December 30, 2024

概括

暴露于颗粒物 (PM) 会通过炎症酶激活引起血管炎症. 抗氧化剂可以减轻这种影响,这表明预防PM相关心血管疾病的目标.

科学领域:

环境健康环境健康
心血管研究研究心血管研究
分子毒理学分子毒理学

背景情况:

环境颗粒物 (PM) 暴露与心血管疾病和血管并发症有关.
颗粒物诱导的血管毒性的机制,特别是短期暴露,需要进一步阐明.

研究的目的:

调查PM及其碳酸核在血管内皮炎症中的作用.
为了确定PM SRM1648a暴露是否激活炎症体并诱导内皮细胞中的氧化应激.

主要方法:

在BALB/c小鼠中短期PM SRM1648a暴露以评估系统性炎症和氧化应激生物标志物.
使用人类静脉内皮细胞 (HUVEC) 和EA.hy926细胞进行体外研究,以检查炎症酶激活途径.
评估还原氧平衡,细胞因子概况,炎症组分 (NLRP3,NLRC4),卡斯巴-1,IL-1β和细胞死亡模式.

主要成果:

在小鼠中,PM SRM1648a暴露改变了氧化还原平衡和细胞因子概况.
在血管内皮细胞中对NLRP3/NLRC4炎症体,卡斯帕酶-1和IL-1β激活的升调.
抗氧化剂治疗 (谷甲单乙烯) 在体外有效降低了氧化应激和炎症酶激活,而灭不是主要的细胞死亡机制.

结论:

PM SRM1648a通过ROS介导的炎症酶激活诱导血管内皮炎症.
颗粒物的碳核是这种炎症反应的关键贡献者.
准ROS和炎症体通路可能提供针对PM诱导的血管损伤的治疗策略.

关键词:

碳黑是一种碳黑.卡斯帕塞斯 (Caspase) 是一个内皮细胞内皮细胞的内皮细胞.在炎症中,一些细胞会发炎.对于PM2.5来说,这是一个很好的例子.热性灭症 (Pyroptosis) 是一种

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