Abstract
BACKGROUND: Fine particulate matter (PM(2.5)), an important component of ambient air pollution, induces significant adverse health effects. MitoQuinone (MitoQ), a mitochondria-targeted antioxidant, has been reported to play a protective role in various diseases. However, the roles of MitoQ in PM(2.5) induced pulmonary toxicity remains to be elucidated. METHODS: All the experiments were performed at Higher Educational Key Laboratory for Translational Oncology of Fujian Province, Putian City, China in 2023. Pulmonary epithelial cells (A549) were pretreated with 4 μM MitoQ for 2 h and exposed to PM(2.5) for 24 h. Cell viability was tested through CCK8 assay. Oxidative stress state and active mitochondria was used to study MitoQ's effect on PM(2.5) induced injury, and cell apoptosis was measured using a flow cytometer and analyzed by Bcl-2 family. RESULTS: MitoQ pretreatment significantly relieved a decreased cell viability, subsequently, MitoQ alleviated ROS production and prevented the reduction of T-AOC and GSH and increased the expression of NF-E2-related factor 2 (Nrf2) and p62 in A549 cells exposed to PM(2.5). MitoQ restored the decreased mitochondrial dysfunction and dynamics disorder and inhibited activated mitochondrial-mediated apoptosis induced by PM(2.5). Furthermore, the decreased ratio of Bcl-2/Bax and expression of Mcl-1 and the enhanced expression of Caspase-3 were reversed by MitoQ pretreatment. CONCLUSION: MitoQ might be regarded as a potential drug to relieve PM(2.5) induced pulmonary epithelial cells damage.