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. 2019 Oct 11;10:1135. doi: 10.3389/fphar.2019.01135

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Copyright © 2019 Wen, Zhang, Liu, Wang, Li, Yang, Wang, Cai, Li and Zhao

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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SAL ameliorates H9c2 cells from DOX-induced decrease on mitochondrial fuel flex. Mitochondrial substrate analysis was determined. During testing, H9c2 cells were treated with 4 μM of etomoxir and 3 μM of BPTES/2 μM of UK5099 in succession. (A) Effects of SAL on fuel dependency in terms of the fatty acid oxidation pathway. (B) Effects of SAL on fuel capacity in terms of fatty acid oxidation pathway and oxidation rates of fatty acids expressed in dependency (C), capacity (D), and flexibility (E) to maintain baseline OCR levels determined with the Seahorse XFp respirometer. ^** P < 0.01 versus control group. ^## P < 0.01 versus DOX group. All data are presented as mean ± SD (n = 3). SAL, salsolinol; DOX, doxorubicin; OCR, oxygen consumption rate.