Lycium barbarum polysaccharide's protective effects against PM_2.5-induced cellular senescence in HUVECs

Fine particulate matter (PM_2.5) exposure is strongly associated with vascular endothelial senescence, a process implicated in cardiovascular diseases. While there is existing knowledge on the impact of Lycium barbarum polysaccharide (LBP) on vascular endothelial damage, the protective mechanism of LBP against PM_2.5-induced vascular endothelial senescence remains unclear. In this study, we investigated the impact of PM_2.5 exposure on vascular endothelial senescence and explored the intervention effects of LBP in human umbilical vein endothelial cells (HUVECs). We found that PM_2.5 exposure dose-dependently reduced cell viability and proliferation in HUVECs while increasing the production of reactive oxygen species (ROS), malondialdehyde (MDA), and hydrogen peroxide (H₂O₂). Additionally, PM_2.5 exposure inhibited the activity of superoxide dismutase (SOD). Notably, PM_2.5 exposure induced autophagy impairments and cellular senescence. However, LBP mitigated PM_2.5-induced cell damage. Further studies demonstrated that correcting autophagy impairment in HUVECs reduced the expression of the senescence markers P16 and P21 induced by PM_2.5. This suggests the regulatory role of autophagy in cellular senescence and the potential of LBP in improving HUVECs senescence. These findings provide novel insights into the mechanisms underlying PM_2.5-induced cardiovascular toxicity and highlight the potential of LBP as a therapeutic agent for improving vascular endothelial health.