PPAR-gamma调节肺上皮细胞中的PFAS介导的炎症性细胞因子
Sadiya Bi Shaikh1, Md Imam Faizan1, Khursheed Ul Islam1
1Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, United States.
Frontiers in pharmacology
|February 19, 2026
概括
和多醇基物质 (PFAS) 通过PPARγ信号传递触发肺炎. 激活这种途径的药物,如罗西格利塔可以减少PFAS诱导的细胞因子释放在肺细胞.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
背景情况:
- 和多甲基物质 (PFAS),包括 perfluorooctanesulfonic 酸 (PFOS),是人类肺部积累的持久性污染物.
- 积累PFAS可能会导致肺炎和免疫失调.
- 氧酶增殖器激活受体玛 (PPARγ) 在PFAS诱导的肺毒性中的作用尚不清楚.
研究的目的:
- 调查PPARγ信号在PFAS诱导的肺炎中的参与.
- 确定PPARγ激活是否可以减轻肺上皮细胞中PFAS诱导的炎症反应.
主要方法:
- 人类支气管上皮细胞 (NHBE) 暴露于带有或没有PPARγ激动剂/对抗剂的PFAS混合物.
- 在BALB/c小鼠中,PFOS被口服两周.
- 测量了细胞因子分泌 (IL-6,IL-8) 和PPARγ/PPARα蛋白水平.
主要成果:
- 暴露于PFAS会增加NHBE细胞中的IL-6和IL-8分泌.
- PPARγ激动剂 (罗西格利塔,皮奥格利塔) 逆转了PFAS诱导的细胞因子增加.
- 在小鼠中,PFAS暴露降低了肺PPARγ蛋白水平,而PPARα保持不变.
结论:
- 由PFAS诱导的促炎细胞因子部分通过PPARγ信号传递进行介导.
- 药理上激活PPARγ可以减弱肺上皮细胞中PFAS诱导的炎症反应.
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