Fig. 4

LCN2 regulated ferroptosis in 661 W photoreceptor cells by modulating the JNK pathway. A, B Phosphokinase array, revealing that treatment with 1 μg/mL rLCN2 for 24 h activated p-JNK expression compared with the vehicle control (Ctrl; PBS), which was validated by western blotting analysis. C‒G Western blotting and quantitative analysis of SLC7A11 and GPX4 protein expression levels in the indicated groups. 661 W cells were preincubated with SP600125 (5 μM) or vehicle (DMSO) for 0.5 h, followed by treatment with or without 1 μg/mL rLCN2 for 24 h. Protein expression levels of p-JNK were normalized to those of JNK and are presented as fold changes. The protein expression levels of JNK, SLC7A11, and GPX4 were normalized to those of β-actin and are presented as fold changes. H MDA levels in the indicated groups. I GSH levels in the indicated groups at 24 h after light exposure (LE). J‒L Western blotting and quantitative analysis, showing that LCN2 knockdown inhibited LE-induced JNK phosphorylation. Protein levels of p-JNK and JNK were normalized to those of JNK and β-actin, respectively, and are presented as fold changes.n= 1 for the phosphokinase array.n= 3 for western blotting, MDA, and GSH measurements per group. *P< 0.05, **P< 0.01. One-way ANOVA followed by Tukey’s post hoc test