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. 2022 Sep 23;13:904314. doi: 10.3389/fphar.2022.904314

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Copyright © 2022 Li, Yan, Zhao, Zhang and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Ferroptosis in H9c2 cardiomyoblasts is activated after sorafenib treatment. (A–C) The mRNA and protein level of Slc7a11 and GPX4. Data are represented as means ± SD for three biological replicates. (D) Representative transmission electron microscopy images (Whole image scale bar = 1 μm, zoomed sections = 250 nm). (E) Intracellular ROS levels were evaluated by DCFH-DA staining. Scale bar = 50 μm. (F) The generation of lipid ROS was determined by the C11-BODIPY probe. Scale bar = 50 μm. (G) JC-1 aggregates show red fluorescence, indicating high mitochondrial membrane potential, and JC-1 monomers show green fluorescence. Scale bar = 50 μm *p < 0.05, **p < 0.01, ***p < 0.001 vs. control group. #p < 0:05, ###p < 0.001 vs. sorafenib group. One-way ANOVA with Tukey’s post hoc test was used for multigroup comparisons.