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. 2020 Sep 15;11(9):756. doi: 10.1038/s41419-020-02948-2

Fig. 5. Acot1 knock-down sensitized cardiomyocytes to DOX toxicity caused by ferroptosis.

Fig. 5

a Realtime-qPCR confirming the efficiency of si-Acot1 #1, #2 comparing with scrambling si-NC. b Western blot confirming the efficiency of si-Acot1 #1, #2 comparing with scrambling si-NC. c Ptgs2 mRNA level in DOX (2 μM, 24 h) treated HL-1 cells transfected with si-Acot1 #1, #2, and si-NC. d Cell viability analysis showing the effect of Acot1 knock-down in DOX (2 μM, 24 h) induced cell death and the protective effect of Fer-1 (10 μM) co-treatment. e The intracellular GSH/GSSG levels showing the effect of DOX (2 μM, 6 h) treated HL-1 cells with or without Acot1 knock-down and the protective effect of Fer-1 (10 μM) co-treatment. f Flow cytometer analysis of C11-BODIPY 581/591 staining showing lipid peroxidation level in DOX (2 μM, 6 h) treated HL-1 cells with or without Acot1 knock-down and the representative fluorescent images showing lipid peroxidation level. Significance in a, c was calculated using the unpaired Student’s t test. Significance in d, e was calculated using the one-way ANOVA test with multiple comparisons between two groups. P value < 0.05 was considered to be significant, and labeled as *P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.001; ns not significant.