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. 2025 Jan 22;66(1):50. doi: 10.1167/iovs.66.1.50

Figure 3.

Figure 3.

DNA-PKcs inhibits erastin-induced ferroptosis. (A, B) The phosphorylation of DNA-PKcs, ATM, and ATR was determined by (A) Western blot and (B) quantitative analysis of phosphorylation of DNA-PKcs after being treated with 20 µM erastin (n = 3) . (C) Cell viability was analyzed by the CCK-8 after iRPE cells were treated with KU-57788 for 24 hours (n = 3). (D, E) The phosphorylation of DNA-PKcs in iRPE cells was determined by (D) Western blot and (E) quantitative analysis (n = 3). (F) Calcein/PI staining revealed PI+ iRPE cells. Scale bar: 50 µm. (G) Quantitative analysis of the proportion of PI+ iRPE cells (n = 6). (H) Cell viability was analyzed by the CCK-8 after iRPE cells were treated with KU-57788 or erasin for 24 hours (n = 3). (I) Peroxidized lipids were detected by BODIPY581/591-C11 staining after cells were treated with KU-57788 or erastin for 12 hours. (J) The production of peroxidized lipids was determined as the ratio of the cells with fluorescence of 510 wave length over the cells with fluorescence of 590 wave length (n = 6). Data are mean ± SD, *P < 0.05, **P < 0.01, ***P < 0.001 using one-way ANOVA and post hoc Bonferroni's test.