To investigate the effect of arctigenin on bronchial epithelial cell injury caused by Pseudomonas aeruginosa (PA) infection and its mechanism.

BEAS-2B cells were randomly divided into control group (conventional culture), PA group (1.50×10⁸ CFU·mL^-1 PA infection), PA+ low dose group (PA combined with 10.00 mmol·L^-1 burdock aglycone), PA+ high-dose group (PA combined with 20.00 mmol·L^-1 burdock aglycone). The expression of inflammatory factors and glutathione (GSH) was detected by kit assay, glutathione peroxidase 4 (GPX4) protein was detected by Western blot assay, and lipid peroxidation levels were detected by immunofluorescence assay.

The IL-6 contents of control group, PA group, PA+ low dose group and PA+ high dose group were (20.43±2.82), (106.28±8.07), (76.66±5.73) and (50.57±3.98) pg·mL^-1, respectively; the GSH contents were (25.95±1.46), (10.59±0.60), (13.98±0.74) and (21.52±2.36) ng·mL^-1, respectively; GPX4 protein expression levels were 0.76±0.06, 0.33±0.05, 0.46±0.05 and 0.62±0.06, respectively; the lipid peroxidation levels were (100.00±4.29)%, (470.91±36.33)%, (331.16±27.04)% and (160.16±18.65)%, respectively. The above indexes in PA group compared with control group, PA+ low dose group and PA+ high dose group were compared with PA group, and the differences were all statistically significant (all P<0.01).

Arctigenin can reduce the inflammation of PA-infected BEAS-2B cells by inhibiting GPX4-related ferroptosis pathway.