Ellagic acid alleviates PM2.5-induced senescence of lung epithelial cells by mediating autophagy.

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.