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. 2019 Nov 12;10:1329. doi: 10.3389/fphar.2019.01329

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Copyright © 2019 Fan, Tang, Ye, Zhu, Dai, Yao and Yao

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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QLQX inhibits ISO-induced myocardial apoptosis and autophagy and involves in regulating the AKT/mTOR pathway in vivo. (A) Representative images of TUNEL staining (×400) for the different groups treated by ISO with or without QLQX. (B) Quantitative analysis of the proportion of TUNEL-positive cells. (C) Representative IHC images of LC3 in rats left ventricles (×100) for the different groups treated by ISO with or without QLQX. (D) Quantitative analysis of integrated optical density of LC3. (E) Representative western blotting bands of LC3I, LC3II, Bcl-2, Bax, p-AKT, AKT, p-mTOR, and mTOR and quantitative analysis of the ratios of LC3II/LC3I, Bcl-2/Bax, p-AKT/AKT, p-mTOR/mTOR by densitometry based on immunoblot images. Data are expressed as mean ± SD, n = 3. ^### p < 0.001 versus control group; *p < 0.05, **p < 0.01, ***p < 0.001 versus ISO group. ISO, isoproterenol; QLQX, Qi-Li-Qiang-Xin.