Abstract:
Objective To investigate whether PM2.5 organic extract can induce ferroptosis in human bronchial epithelial cells.
Methods PM2.5 organic extract was obtained using the Soxhlet extraction method and used as the poisonous substance. BEAS-2B cells were exposed to different doses of PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 organic extract.
Conclusion The organic extract of PM2.5 may induce cellular ferroptosis, resulting in damage to respiratory system cells, and consequently, exerting potential health impacts on lung tissues.
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