Amino-modified polystyrene nanoplastics induce endothelial pyroptosis and pro-atherogenic cellular responses.

Nanoplastics (NPs) contamination in food has become a critical issue due to the potential impacts on human health. Currently, NPs have the potential to induce cardiovascular damage, but the exact mechanism at the cellular level is unclear. In addition, environmental factors can modify the surface functional groups of NPs, among which amino-modified NPs (NH2-NPs) significantly affect their toxicity. This study aimed to investigate the effects of NPs with different particle sizes and amino modifications on human umbilical vein endothelial cells (HUVECs). Results demonstrated that 20 nm NH2-NPs exerted the most significant effect on the expression levels of pyroptosis-related proteins. The pyroptosis inhibitor VX-765 reduced PI-positive cells and the expression of pyroptosis proteins in HUVECs, supporting a critical role of pyroptosis in NH2-NPs-induced injury. Subsequently, exposure to 20 nm NH2-NPs resulted in HUVECs injury, which promoted the recruitment of human acute monocytic leukemia (THP-1) cells, with increased adhesion, migration, and lipid accumulation. These findings indicated that PS-NPs induced injury in HUVECs by NF-κB/NLRP3/GSDMD-mediated pyroptosis pathway and influenced THP-1 cells adhesion, migration, and foam cell formation. This study provided insights into the vascular toxicity mechanisms of PS-NPs and highlighted the critical role of surface chemical modifications in modulating their toxicological effects.