Résumé
Objective To investigate the effect of PM2.5 airborne particulate matter with a mean diameter of less than 2.5μm exposure on autophagy and explore the links between autophagy and apoptosis in human lung cancer cells(A549). Methods A549 cells were exposed to 100μg/mL PM2.5 with or without 3-MA(autophagy inhibitor)for various periods of 0、2、4、12 or 24 hrs. Autophagy in A549 cells was assessed by determining the lev-el of LC3(a known autophagy marker)using confocal microscopy. The level of microtubule-associated protein 1 light chain 3(LC3) Ⅱ conversion and Bax (a pro-apoptotic protein) was detected by western blotting. Results The expression of LC3 and the ratio of LC3-II/LC3-I in A549 cells was significantly increased and Bax was signifi-cantly decreased following exposure to PM2.5100 μg/mL for 24 h in a time-dependent manner(P < 0.05). After treated with 100 μg/mL PM2.5,the formation of LC3 in A549 cells as evidenced by the intensity of intracellular fluorescence was significantly increased ,and autophageosomes were observed around nucleus in A549 cells. Fur-thermore blockage of autophagy by 3-MA led to a significant increase in the pro-apoptotic protein Bax. Conclu-sion PM2.5 exposure induces autophagy which may protect against apoptosis induced by PM2.5 in A549 cells.
Résumé
Lots of evidence show a correlation between air pollution and chronic respiratory diseases, of which the effect of particulate matter is the most concerned.It is the current research hotspot that respiratory diseases in both children and adults are closely related with atmospheric pollution levels.The influence mechanisms of atmos-pheric pollution on respiratory diseases include oxidative stress, inflammation, genetic damage, etc.This paper made a review of the latest advances s on the pathogenesis of chronic respiratory diseases caused by atmospheric particulates PM2.5 .