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丁甲对血管内皮的作用:体外和体内证据
Bojana Stanic1, Dunja Kokai1, Jelena Markovic Filipovic1
1University of Novi Sad, Faculty of Sciences, Department of Biology and Ecology, Serbia.
Chemico-biological interactions
|June 29, 2024
概括
迪布甲酸盐 (DBP) 暴露会影响血管内皮细胞,影响迁移,粘附和管形成. 在体内研究表明,DBP改变了老鼠的大动脉形态,突出显示了这种常见化学物质的潜在风险.
科学领域:
- 毒理学和环境健康
- 血管生物学和内皮功能
背景情况:
- 双甲酸 (DBP) 是一种无处不在的化学物质,在消费者和个人护理产品中发现.
- 了解血管内皮对DBP的反应至关重要,因为它对人类的广泛暴露.
- 之前的研究表明,与甲酸盐暴露相关的潜在健康风险.
研究的目的:
- 为了研究DBP对人类内皮细胞 (ECs) 和老鼠大动脉的影响.
- 在不同的DBP暴露场景下检查血管功能,包括EC迁移,粘附和管形成.
- 阐明参与DBP诱导的内皮功能障碍的信号通路.
主要方法:
- 短期 (24小时) 和长期 (12周) 在体外暴露EA.hy926细胞对不同DBP度.
- 在28天和90天内,大鼠体内暴露于食物中的DBP.
- 评估EC迁移,粘附于凝,管形成,大脑形态和关键信号通路的激活 (例如,eNOS,Akt).
主要成果:
- 短期的DBP暴露增加了EC迁移和降低了粘附力.
- 长期的DBP暴露显示了EC迁移的短暂增加,对粘附和管形成的双向影响,以及氧化 (NO) 生产的持续增加.
- 在体内,90天的DBP暴露降低了大动脉壁与光膜的比率,并增加了老鼠大动脉EC中的eNOS和Akt酸化.
结论:
- 短期和长期的DBP暴露在体外显著影响内皮细胞功能,如迁移,粘附和管形成.
- 在体内,DBP暴露导致大动脉形态的有害变化.
- eNOS-NO和Akt信号通路被认为是DBP血管效应的关键媒介,特别是在长期暴露场景中.
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