Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway

Polystyrene nanoplastics(PS-NPs) in the atmosphere can be inhaled because of their small size. They will be deposited deep in the alveoli. This poses a major threat to respiratory health. The molecular mechanism of acute lung injury caused by them has not yet been fully clarified. This study established an acute mouse nasal drip model. The dose is 50 and 100 mg/kg respectively, and it can be used continuously for seven days. We evaluated the lung tissue damage and the activation of the cGAS-STING-NLRP3 pathway. The measurements carried out include oxidative stress markers and key apoptosis and cell pyrotosis proteins. Molecular docking simulation was also carried out. The results show that PS-NPs exposure leads to oxidative damage and apoptosis. This work systematically proved that inhaled PS-NPs triggers acute lung injury through the cGAS-STING-NLRP3 pathway. This discovery promotes the understanding of the toxicity mechanism of nanoplastics. It also identified this axis as a key target for future risk assessment and targeted treatment.