在老鼠中,SiO2颗粒通过ROS/Keap1/Nrf2信号通路调节NLRP3,从而诱导肺纤维化
Shuang Li1, Wei-Lei Gong2, Lin Liu3
1Department of Public Health, Jining Medical University, Jining, China; Shandong Weixuankang Technology Innovation Co. LTD, Tai An, China.
概括
颗粒通过激活ROS/Keap1/Nrf2通路引起肺纤维化,这反过来激活NLRP3炎症酶. 用NAC抑制ROS可以减少这种激活和纤维化.
科学领域:
- 肺部医学 肺部医学
- 毒理学 毒理学 毒理学
- 免疫学 免疫学 免疫学
背景情况:
- 病的发病包括依赖ROS的NLRP3炎症酶激活.
- SiO2诱导的ROS激活NLRP3的精确机制尚未完全理解.
研究的目的:
- 阐明二氧化 (SiO2) 颗粒诱导ROS和激活NLRP3炎症体的机制.
- 调查Keap1/Nrf2信号通路在SiO2诱导的肺纤维化中的作用.
主要方法:
- 通过内SiO2灌注建立了小鼠化病模型.
- 服用N-乙半氨酸 (NAC) 抑制ROS并评估其剂量依赖的影响.
- 分析了肺病理,ROS水平,以及Keap1/Nrf2和NLRP3炎症组分的表达.
主要成果:
- 病模型大鼠表现出ROS水平的增加,激活Keap1/Nrf2信号,以及NLRP3炎症酶激活.
- 根据剂量,NAC治疗抑制了ROS,Keap1/Nrf2通路激活,NLRP3炎症组和肺纤维化.
- 这些发现表明ROS/Keap1/Nrf2通路在调解SiO2诱导的NLRP3激活方面起着至关重要的作用.
结论:
- SiO2颗粒通过ROS/Keap1/Nrf2信号通路激活NLRP3炎症体来诱导肺纤维化.
- 向ROS/Keap1/Nrf2通路和NLRP3炎症酶是一种潜在的治疗策略.
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