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. 2022 Dec 30;132(2):208–222. doi: 10.1161/CIRCRESAHA.122.321153

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© 2023 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 4. — Overexpression of ASPP1 aggravates H/R-induced damage in neonatal mouse ventricular cardiomyocytes (NMVCs). A, The efficiency of ASPP1 overexpression plasmid in NMVCs by Western blot (Student t test); n=6. B, LDH release (1-way ANOVA, followed by Tukey post hoc multicomparisons test); n=6. C, Apoptosis of NMVCs detected by TUNEL (TdT-mediated dUTP nick end labeling) assay (1-way ANOVA, followed by Tukey post hoc multicomparisons test); n=6. Scale bar=50 μm. Green, TUNEL -positive cells; blue, DAPI. D, Mitochondrial membrane potential of NMVCs by JC-1 assay (1-way ANOVA, followed by Tukey post hoc multicomparisons test); n=6. Scale bar=50 μm. E, Caspase-3 activity in NMVCs by ELISA assay (1-way ANOVA, followed by Tukey post hoc multicomparisons test); n=6. F and G, The protein levels of Bcl2 (F) and Bax (G) detected by Western blot (1-way ANOVA, followed by Tukey post hoc multicomparisons test); n=6. ASPP1 indicates apoptosis stimulating of p53 protein 1; Bax, Bcl2-associated X; DAPI, 4′,6-diamidino-2-phenylindole; H/R, hypoxia/reoxygenation; and LDH, lactate dehydrogenase.