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. 2019 Jul 12;10:779. doi: 10.3389/fphar.2019.00779

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Copyright © 2019 Mao, Vincent, Chen, Zhang and Hinek

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Sustained activation of autophagy in hearts treated with STS. (A) Electron micrographs of autophagosomes in the ischemic border zone of heart myocardium 4 weeks after left anterior descending artery ligation. Original magnification ×5,000; (scale bars = 2 µm). Quantitative analysis of autophagosome number is shown in right panel. (B) Representative images of LC3 dots in ischemic border zone of post-MI heart; green, LC3; blue, 4′,6-diamidino-2-phenylindole-stained nuclei; red, myoglobin-positive cardiomyocytes; original magnification ×200 (scale bar = 20 µm). (C) Western blots with densitometric analysis (left panel) of autophagy-related LC3 and p62 protein expression in hearts. Graphs (right panel) show the intensity of each band in fold change: the LC3-II/LC3-I ratio and p62 expression. ^# P < 0.05 versus sham; *P < 0.05 versus vehicle; ^& P < 0.05 versus STS. Veh, vehicle; STS, sodium tanshinone IIA sulfonate; Cq, chloroquine.