NLRP3 inflammasome activation is associated with PM2.5-induced cardiac functional and pathological injury in mice

Growing evidences indicate that inflammation induced by PM2.5 exposure has been considered as a major driving force for the development of cardiovascular diseases. However, the mechanisms underlying PM2.5-induced cardiac injury remain unclear. This study aims to investigate the role of NLRP3 inflammasome in PM2.5-induced cardiac functional and pathological injury in mice. In this study, BALB/c mice were intratracheally instilled with PM2.5 suspension (4.0 mg/kg BW) for 5 days to set up a cardiac injury model, which was evaluated by electrocardiogram monitoring, HE and Masson staining. Then, the effects of PM2.5 on the expression of alpha-SMA, NLRP3, IL-1 beta, and IL-18 proteins and the activation of caspase-1 and IL-1 beta were investigated. The results showed that PM2.5 exposure induced characteristic abnormal ECG changes such as the abnormality of heart rhythm, tachycardia, and T-wave reduction. Inflammatory cell infiltration and fibrosis were observed in the heart tissues of PM2.5-exposed mice. Meanwhile, PM2.5 exposure increased the expression of alpha-SMA. And, NLRP3 activation-associated proteins of NLRP3, IL-1 beta, IL-18, Cleaved caspase-1 p10, and Cleaved IL-1 beta were upregulated in heart tissue of PM2.5-induced mice. In summary, PM2.5 exposure could induce cardiac functional and pathological injury, which may be associated with the activation of NLRP3 inflammasome.