PM induced lung injury through upregulating ROS-dependent NLRP3 Inflammasome-Mediated Pyroptosis.

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.