Cooking oil fume-derived PM2.5 induces apoptosis in A549 cells and MAPK/NF-κB/STAT1 pathway activation

Cooking oil fumes (COFs) are the major sources of indoor air pollution in Asia. It is well known that alveolar cells are key participants in the development of respiratory system; however, it still remains unknown whether alveolar cells are affected by COFs. Therefore, the present study investigated the effects of COFs on alveolar cells (A549 cells) and illuminated its apoptotic mechanism in response to COF-PM2.5 exposure. When A549 cells were exposed to COF-PM2.5, cell viability was substantially decreased, while the generation of ROS increased, and LDH levels and CCK-8 levels gradually changed within a dose-dependent manner. The nitrite concentration in the supernatants was augmented, while the SOD activity and GSH recycling were decreased upon COF-PM2.5. Moreover, COF-PM2.5 treatment increased mRNA levels of COX-2, inducible NO synthase, and TNF-alpha, and Elisa assay suggested that secretory proteins IL-6 and TNF-alpha were also increased. Furthermore, the Bax/Bcl-2 mRNA ratio was increased, and cleaved caspase-3 protein was activated in the A549 cells. Strikingly, COF-PM2.5 induced the phosphorylation of STAT1 at Tyr701/Ser727 and activation of NF-kappa B and ERK1/2, p38, and JNK of the MAPK pathway. In short, our study suggested that COF-PM2.5 resulted in inflammation, apoptosis, and cell damage in A549 cells, which might be modulated via the activation of MAPK/NF-kappa B/STAT1 pathway.