Fig. 3: Vitamin K protects RPE from ferroptosis in vitro.
From: The role of vitamin K and its antagonist in the process of ferroptosis-damaged RPE-mediated CNV
A, C Morphological changes of ARPE-19 cells were observed by optical microscopy. B, D Cell viability of ARPE-19 cells was detected by CCK-8 assays. A, B ARPE-19 cells were treated with erastin (5 μM) for 0, 4, 8, 24, 36 and 48 h, respectively. C, D ARPE-19 cells were treated with erastin at concentrations of 0, 1, 3, 5, 10, 20 μM, respectively, for 24 h. E, F Cell viability of ARPE-19 cells was detected by CCK-8 assays. E ARPE-19 cells were treated with erastin (5 μM) for 24 h after pretreatment with/without VK (1, 5, 10, 25 μM) or Fer-1 (10 μM) for 1 h. F ARPE-19 cells were treated with VK at concentrations of 0.1,1, 10, 25, 50, 100 μM respectively for 24 h. G–I ARPE-19 cells were treated with erastin (5 μM) for 24 h or J 4 h after pretreatment with/without VK (10 μM) or Fer-1 (10 μM). G, K Cell survival/death and cell mortality qualification of ARPE-19 cells were detected by live/dead staining (Calcein AM: Live cells; PI: Dead cells). H, L ROS and I, M lipid ROS production in ARPE-19 cells were detected using a DCFH-DA-ROS assay kit and BDP 581/591 C11 fluorescent probe (Green: oxidized BDP 581/591 C11; Red: non-oxidized BDP 581/591 C11) respectively. J, N Changes in mitochondrial membrane potential in ARPE-19 cells were evaluated by mitochondrial membrane potential probe JC-1 (Red: high potential; Green: low potential). The data represent the averages of three independent experiments. Data shown are mean ± SD; one-way ANOVA with Bonferroni correction; **P < 0.01. Scale bars: 500 μm (A, C); 100 μm (G); 50 μm (H); 20 μm (I, J); 5 μm (J).
