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. 2022 Apr 5;52:102311. doi: 10.1016/j.redox.2022.102311

Fig. 2.

Fig. 2

Mfn2 overexpression restored mitochondrial fusion and inhibited mitochondria-dependent apoptosis in the Dox-treated cardiomyocytes. (A) Representative blots and quantitative data of Mfn2. (B) MitoTracker Red-stained mitochondrial morphology images and quantitative data of mean mitochondrial size. Original magnification × 600. (C) Quantitative data of mitochondrial number per cell. (D) Relative cell viability. (E) Lactate dehydrogenase (LDH) release determined in cell supernatant. (F) Relative activity of caspase 3 expressed as a fold change compared with Con + Ad-EV. (G) Representative images of TUNEL and DAPI staining. (Quantitative data are presented in H). Original magnification × 400. (H) Quantitative data of the apoptotic index. (I) Representative images of mitochondrial membrane potential stained by JC-1. (Quantitative data are presented in J). Original magnification × 200. (J) Quantification of mitochondrial membrane potential. (K-L) Representative blots and quantitative data of cytosolic cytochrome c (cyt-c). n = 6 independent experiments per group in Figure B–J. The blotting experiments were conducted 3 times independently per group in Figure A and Figure K–L. One-way ANOVA with Turkey's multiple comparison test was used. *P < 0.05, **P < 0.01, ***P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)