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. 2021 Mar;9(6):479. doi: 10.21037/atm-21-503

Figure 2.

Figure 2

CaMEK transduction ameliorated cell apoptosis and improved mitochondrial morphology in aging hearts with MI. (A,B) Ischemia induced oxidative stress, which was attenuated by CaMEK transduction. ROS detection was carried out through DHE staining. Typical images were shown in (A), and quantified results were shown in (B). (C,D) SOD activity and ATP level in aging hearts with MI were shown in (C) and (D), respectively. (E,F) CaMEK transduction improved mitochondrial morphology, as detected by electron microscope in aging hearts with MI. Typical images were shown in (E), and quantified results were shown in (F). (G,H,I,J) The content of Mfn1, Mfn2, and OPA1 in aging hearts with MI. Representative immunoblots were shown in (G), and quantified results were shown in (H,I,J). (K,L,M,N,O) The content of Drp1, Drp1 phosphorylation, and Fis1 in aging hearts with MI. Representative immunoblots were shown in (K), and quantified results were shown in (L,M,N,O). (P,Q) The content of Bcl-2 and Bax in aging hearts with MI. Representative immunoblots were shown in (P), and quantified results were shown in (Q). (R,S) CaMEK transduction decreased cell apoptosis in aging hearts with MI. Typical images of heart sections stained with TUNEL were shown in (R), and TUNEL-positive nuclei (white arrows) were counted in several randomly selected fields. Quantitative analysis of apoptotic index was shown in (S). Data were presented as the mean ± SD (n=3). *P<0.05, **P<0.01. ROS, reactive oxygen species; DHE, dihydroethidium; SOD, superoxide dismutase; ATP, adenosine triphosphate; Mfn1, mitofusin 1; Mfn2, mitofusin 2; OPA1, optic atrophy 1; Drp1, dynamin-related protein-1; Fis1, fission protein 1; Bcl-2, B-cell lymphoma-2; Bax, BCL2 associated X; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.