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. 2024 Jan 29;70:103066. doi: 10.1016/j.redox.2024.103066

Fig. 6.

Fig. 6

H2S inhibited DOX-induced cardiomyocyte ferroptosis via regulating SLC7A11/GSH/GPx4 pathway.

A-C, Representative blots and quantitative analysis of SLC7A11 and GPx4 protein levels in heart tissues (n = 3). D, the ratio of the GSH and GSSG in heart tissues (n = 6). E-G, Representative blots and quantitative analysis of SLC7A11 and GPx4 protein levels in heart tissues (n = 3). H, the ratio of the GSH and GSSG in heart tissues (n = 6). I–K, Representative blots and quantitative analysis of SLC7A11 and GPx4 protein levels in H9c2 cells (n = 3). L, the ratio of the GSH and GSSG in H9c2 cells (n = 3). M, The glutamate levels of supernatants from cultured H9c2 cells (n = 3). N–P, Representative blots and quantitative analysis of SLC7A11 and GPx4 protein levels in H9c2 cells (n = 3). Q, the ratio of the GSH and GSSG in H9c2 cells (n = 3). R, The glutamate levels of supernatants from cultured H9c2 cells (n = 3). The data are presented as the Mean ± SD. For panel F–H, *p < 0.05 and ***p < 0.001 vs. Vehicle group at the same genetic background; #p < 0.05, ##p < 0.01 and ###p < 0.001 vs. DOX group of Csef/f/cre−; &&&p < 0.001 vs. DOX group of Csef/f/cre+. For the rest of panels, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Vehicle group; ##p < 0.01 and ###p < 0.001 vs. DOX group; @p < 0.05 and @@p < 0.01 vs. siNC + DOX group; $$$p < 0.001 vs. siCse + DOX group.