吸入含有环境持久性自由基的颗粒物会诱导通过空气-血液界面的AhR激活介导的内皮功能障碍
Ankit Aryal1, Ashlyn C Harmon1, Kurt J Varner2
1Department of Comparative Biomedical Sciences, Louisiana State University School of Veterinary Medicine, Baton Rouge, Louisiana 70803, USA.
概括
吸入持久性自由基的颗粒物会激活肺细胞中的受体,导致整个身体的血管功能障碍. 这一途径涉及基碳化合物受体 (AhR) 的激活和介质释放.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 肺部医学 肺部医学
背景情况:
- 有环境持久性自由基 (EPFR) 的颗粒物 (PM) 由不完全燃烧产生的.
- 在小鼠中吸入EPFR会损害内皮依赖的血管扩张.
- 在膜II型 (AT-II) 细胞中,烯碳化合物受体 (AhR) 的激活与EPFR效应有关.
研究的目的:
- 调查AT-II细胞中的AhR激活是否驱动全身介质释放,导致外围内皮功能障碍.
- 确定AT-II细胞AhR在EPFR诱导的内皮功能障碍和氧化应激中的作用.
主要方法:
- 在雄性和雌性小鼠的AT-II细胞中抑制AhR.
- 暴露于EPFR或过空气1天或5天.
- 测量血管松,eNOS表达,内甲蛋白-1,VCAM-1,eNOS,以及氧化应激标志物.
主要成果:
- 在对照小鼠中,EPFR暴露减少了内皮依赖血管松的59%和eNOS表达的50%.
- AT-II AhR激活增加了肺内甲蛋白-1 mRNA和血水平.
- 暴露于EPFR导致氧化和化应激标志物增加,这种方式取决于AT-II AhR.
结论:
- 在AT-II细胞中的AhR激活调解了EPFR诱导的肺周边内皮功能障碍.
- 这种功能障碍可能通过调解剂的全身释放而发生.
- 在EPFR引起的氧化和化应激中,AT-II细胞的AhR起着至关重要的作用.
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