College of Medical Laboratory, Dalian Medical University, Dalian 116044, Liaoning Province, China; The Second People's Hospital Of Quzhou, Zhejiang Province, China.
College of Medical Laboratory, Dalian Medical University, Dalian 116044, Liaoning Province, China.
Immunobiology. 2022 May;227(3):152207. doi: 10.1016/j.imbio.2022.152207. Epub 2022 Mar 16.
The main cause of air pollution is PM, which directly causes lung injury through respiration. Oxidative stress and inflammation are considered to be the key mechanism of cell damage. Pyroptosis is a process of the programmed death of inflammatory cells and as a dangerous endogenous signal, it is widely involved in different inflammatory diseases. However, few studies have been conducted on PM exposure and cell pyroptosis. In this study, we aimed to investigate the effect of PM on apoptosis, pyroptosis and cell cycle arrest regulated by reactive oxygen species production. Balb/c mice were exposed to PM dynamically and verified by the RAW264.7 cells in vitro. The results showed the activation of NF-κB and NLRP3 inflammasome and the release of IL-1β and reactive oxygen species were caused by exposure to PM. The maturation of IL-1β relied on Caspase-1, and the active Caspase-1 was related to cell pyroptosis. Oxidative stress, inflammation, apoptosis and pyroptosis all affected the cell cycle. This study describes a potentially important mechanism of PM-induced lung damage that PM promotes lung injury via upregulating ROS-NLRP3-mediated the RAW264.7 cells pyroptosis.
空气污染的主要原因是 PM，它通过呼吸直接导致肺部损伤。氧化应激和炎症被认为是细胞损伤的关键机制。细胞焦亡是炎症细胞程序性死亡的过程，作为一种危险的内源性信号，广泛参与不同的炎症性疾病。然而，关于 PM 暴露与细胞焦亡的研究较少。在这项研究中，我们旨在研究 PM 对活性氧产物调控的细胞凋亡、焦亡和细胞周期停滞的影响。通过动态暴露 Balb/c 小鼠和体外 RAW264.7 细胞进行验证。结果表明，PM 暴露会激活 NF-κB 和 NLRP3 炎性小体，并释放白细胞介素-1β和活性氧。白细胞介素-1β的成熟依赖于半胱天冬酶-1，而活性半胱天冬酶-1与细胞焦亡有关。氧化应激、炎症、凋亡和焦亡都会影响细胞周期。本研究描述了 PM 诱导肺损伤的一个潜在重要机制，即 PM 通过上调 ROS-NLRP3 介导的 RAW264.7 细胞焦亡促进肺损伤。
