Skip to main content
. 2024 Jan 29;70:103066. doi: 10.1016/j.redox.2024.103066

Fig. 5.

Fig. 5

Cardiac knockout of Cse gene in mice or knockdown Cse gene in H9c2 cells aggravated DOX-induced ferroptosis.

A and B, MDA level in plasma and heart tissues (n = 6). C, The expression levels of Ptgs2 mRNA in heart tissues (n = 6). D, Cell viability of H9c2 cells (n = 3). E, The expression levels of Ptgs2 mRNA in H9c2 cells (n = 6). F and G, Representative images and quantification of intracellular lipid peroxide in H9c2 cells (n = 3). J, Representative images of intracellular ROS level detected by cell ROS fluorescent probe (Red) in H9c2 cells, and the quantitative analysis of the fluorescence intensities were shown in H (n = 3). K, Representative images of mitochondrial membrane potential detected by JC-1 fluorescent probe in H9c2 cells, and the quantitative analysis was established as the ratio of the JC-1 Monomers (Green) and JC-1 Aggregates (Red) in I (n = 3). L-N, Real-time oxygen consumption rates (OCR) and calculated basal and maximal respiration rates in H9c2 cells (n = 3). The data are presented as the Mean ± SD. For panel A-C, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Vehicle group at the same genetic background; ###p < 0.001 vs. DOX group of Csef/f/cre; &&&p < 0.001 vs. DOX group of Csef/f/cre+. For panel D-N, *p < 0.05 and ***p < 0.001 vs. Vehicle group; @p < 0.05, @@p < 0.01 and @@@p < 0.001 vs. siNC + DOX group; $$$p < 0.001 vs. siCse + DOX group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)