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. 2019 May 14;2019:5406468. doi: 10.1155/2019/5406468

Figure 4.

Figure 4

Effects of SPD on mitochondrial quantity and quality, mitochondrial function, and MnSOD expression in the myocardium of neonatal offspring and on mitochondrial ROS production and membrane potential in primary cardiomyocytes (NRCMs). (a) TEM of myocardial ultrastructure of normal (control), hypoxia (Hpx), SPD-treated (Hpx-Spd), and SPD+polyamine synthesis inhibitor- (Hpx-Spd-DMFO-) treated groups (magnification, 10,000x). (b) Representative TEM images showing ultrastructural changes in the myocardial mitochondria of each group (magnification, 30,000x). (c, d) Quantification of the area of cells occupied by mitochondria (%) and the quantitative mitochondrial area (n = 10). (e–g) Mitochondrial function was evaluated based on mitochondrial state 3 (e) and state 4 (f) oxygen consumption and the respiratory control rate (RCR) (g) in cardiac mitochondria isolated from 7-day-old offspring hearts (n = 10). (h) The expression ratio of SOD proteins in isolated mitochondria detected by western blotting. (i) Quantification of the protein levels (n = 4). (j) Detection of superoxide production in myocardial mitochondria of NRCMs by the MitoSOX Red fluorescent probe. (k) Statistical quantification of the average fluorescence intensity of MitoSOX Red (n = 6). (l) Detection of mitochondrial membrane potential (ΔΨm) of NRCMs by the JC-1 fluorescent probe. (m) Statistical analysis of the ratio of red to green fluorescence (n = 6). Data are shown as the mean ± SEM. ∗ P < 0.05 versus control, # P < 0.05 versus the Hpx group, and △ P < 0.05 versus the Hpx-Spd group.