Abstract
Fine particulate matter (PM(2.5)) exposure is significantly linked to lung epithelial cell senescence, and autophagy dysfunction being a key contributor to the aging process. Although the anti-aging properties of ellagic acid (EA) are well-documented, its specific protective effect on PM(2.5)-induced lung epithelial cell senescence still needs to be studied in depth. To investigate the impacts of PM(2.5) on autophagy and senescence in lung epithelial cells, 16HBE and A549 cells were exposed to PM(2.5) suspension. Additionally, to explore the potential intervention effect of EA, cells were pretreated with EA before exposure to PM(2.5) suspension. Cell morphology, proliferation, senescence-related markers, senescence-associated secretory phenotype (SASP), and autophagy-related markers were then assessed. Our results showed that the proliferation of 16HBE and A549 cells were inhibited and autophagy dysfunction and senescence were induced under PM(2.5) exposure. However, pretreatment with EA can significantly improve the obstruction of autophagy flux caused by PM(2.5), thereby effectively alleviating cell senescence. This study reveals the mechanism by which PM(2.5) induces senescence in lung epithelial cells and confirms the protective role of ellagic acid in this process.