Low-Dose Radiation Reduces Doxorubicin-Induced Myocardial Injury Through Mitochondrial Pathways

Figure 1.. Animal disposal process.

Figure 2.. Transmission electron micrograph of myocardial mitochondria (×7500) in different groups. (A) Cardiomyocytes from the Control group showing normal myocardial ultrastructure with regularly arranged mitochondria. (B) Cardiomyocytes from the LDR group showing normal myocardial ultrastructure, and the number of mitochondria was increased. (C) Cardiomyocytes from the DOX group showing large vacuoles and damaged mitochondrial structures. (D) Cardiomyocytes from the LDR-72 h-DOX group showing relatively normal myocardial ultrastructure and slight injury of mitochondria.

Figure 3.. Gene expression profile. (A) Differential gene expression between LDR and Control groups. (B) Differential gene expression between DOX and Control groups. (C) Differential gene expression between the LDR-72 h-DOX and LDR groups. (D) Differential gene expression between LDR-72 h-DOX and DOX groups.

Figure 4.. GO analysis in different groups. (A) GO analysis of differential genes between Control and DOX groups. (B) GO analysis of differential genes between DOX and LDR-72 h-DOX groups.

Figure 5.. LDR pre-treatment could mitigate the mitochondrial deficiency induced by DOX in the hearts of mice. (A) Mitochondrial complex I activity. (B) Mitochondrial complex II activity. (C) Mitochondrial complex III activity. (D) Mitochondrial complex IV activity. (E) Mitochondrial complex V activity. (F) ATP concentration (*P < .05, **P < .01).

Figure 6.. Expression of mitochondrial complex-relative proteins NDUFV1, ATP5f1, and CYC1 (A) Western blot images. (B) Relative optical density (*P < .05, ***P < .005).

Figure 7.. Protective mechanism of LDR pretreatment on DOX via mitochondrial pathways.