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

Fig. 4.

Fig. 4

Mfn2 protected the cardiomyocytes against Dox-induced injury via enhancing mitochondrial fusion and oxidative metabolism. The cardiomyocytes were treated with lentivirus expressing Drp1 (LV-Drp1) or Rote/Anti A (Rote 0.1 μM + Anti A 1 μM) before the transfection of adenoviruses encoding the Mfn2 gene (Ad-Mfn2) under Dox condition. (A) Relative cell viability. (B) Lactate dehydrogenase (LDH) release in cell supernatant. (C) Relative activity of caspase 3 expressed as a fold change compared with Dox. (D) Quantitative data of relative mitochondrial ROS fluorescence density. (E) Representative images of mitochondria-derived superoxide production stained with MitoSOX (upper, quantitative data are presented in D) and MitoTracker Red-stained mitochondrial morphology (bottom, quantitative data are presented in F–G). Original magnification × 600. (F) Quantitative data of mean mitochondrial size in the cardiomyocytes. (G) Quantitative data of mitochondrial number per cell. (H–I) Quantitative data of mitochondrial complex I and III activity. n = 6 independent experiments per group in Figure A–I. One-way ANOVA with Turkey's multiple comparison test was used. ***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.)