Abstract: In this study, we examined whether ferulic acid (FA) could protect against PM2.5-induced mitochondrial damage in A549 cells and explored the underlying mechanism. The cells were treated with PM2.5 (240 μg/mL) with and without the addition of 80 mmol/L FA. The contents of reactive oxygen species (ROS) were determined by flow cytometry using MitoSOX Red specific probe. Apoptosis was detected by flow cytometry with Annexin-V/PI method. Mitochondrial membrane potential was detected by flow cytometry with JC-1 staining. The activity of mitochondrial membrane channel pore was tested by mitochondrial permeability transition pore (mPTP) kit. The expression of caspase-3, caspase-9, manganese superoxide dismutase (MnSOD), and peroxisome proliferators-activated receptor-γ-coactivator-1α (FGC-1α) were detected by Western blotting. The results showed that, compared with the blank control group, the level of ROS and the expression of caspase-3 and caspase-9 in mitochondria, as well as the apoptosis rate of A549 cells induced by PM2.5 were increased. The membrane potential and the activity of mPTP in mitochondria of A549 cells induced by PM2.5 were decreased as well as the expression of PGC-1α and MnSOD. The pre-treatment of FA could prevent the increased mitochondrial ROS, apoptosis rate and expression of caspase-3 and caspase-9, and the decreased mitochondrial membrane potential, mPTP activity, and expression of PGC-1α and MnSOD caused by PM2.5. Therefore, FA had a significant protective effect on PM2.5-induced mitochondrial damage in A549 cells.

Key words: ferulic acid, PM2.5, A549 cells, mitochondria, damage, protective effect