A study on bronchial epithelial cell injury induced by PM_2.5 organic extracts through ferroptosis

Objective To investigate whether PM_2.5 organic extract can induce ferroptosis in human bronchial epithelial cells.

Methods PM_2.5 organic extract was obtained using the Soxhlet extraction method and used as the poisonous substance. BEAS-2B cells were exposed to different doses of PM_2.5 organic extract (2.5, 5, 10, and 20 μg/mL) to establish a poisoning model with 0.1% DMSO solution as the control solvent. The ferroptosis inhibitor ferrostatin-1 (Fer-1) was used to establish an intervention model. The viability of BEAS-2B cells exposed to PM_2.5 organic extract as well as malondialdehyde and glutathione levels were evaluated using spectrophotometry. The intracellular levels of Fe2+, reactive oxygen species, and lipid peroxidation were measured using fluorescence methods. The expression levels of ferroptosis-related genes GPX4, SLC7A11, ACSL4, FTL, and TFRC were detected using qRT-PCR.

Results Compared to the control group, BEAS-2B cells exposed to 10 μg/mL PM_2.5 organic extract for 24 h showed significant increases in the concentrations of Fe²⁺, reactive oxygen species, lipid peroxidation, and malondialdehyde. However, the concentration of glutathione decreased significantly. qRT-PCR showed that exposure to 20 μg/mL of PM_2.5 organic extract significantly downregulated the expression of GPX4 but significantly upregulated SLC7A11, ACSL4, FTL, and TFRC. In the intervention experiment, the ferroptosis-specific inhibitor Fer-1 was able to significantly improve the injury caused by PM_2.5 organic extract.

Conclusion The organic extract of PM_2.5 may induce cellular ferroptosis, resulting in damage to respiratory system cells, and consequently, exerting potential health impacts on lung tissues.