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. 2017 Oct 30;8:775. doi: 10.3389/fphar.2017.00775

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Copyright © 2017 Chen, Xu, Zhang, Li, Cui, Li, Chang, Tang, Xu, Tian, Huang, Xu, Jin and Yang.

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) or licensor 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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TXL attenuated myocardial reperfusion injury by promoting the expression of p70s6k1 and increasing the phosphorylation of p70s6k1 in vivo. (A). Myocardial infraction size assessed by Evans blue/TTC double staining (n = 8–9 in each group; rapamycin alone did not affect the infract size after I/R, data not shown). (B) The apoptosis of cardiac cells evaluated by TUNEL/DAPI double staining (n = 4 in each group TUNEL positive cells are indicated by white arrows). (C) The effects of TXL on the protein levels of total p70s6k1 and phosphorylated p70s6k1 in myocardium (n = 4 in each group). ^*P < 0.05 vs. Sham; ^#P < 0.05 vs. I/R; ^$P < 0.05 vs. I/R+TXL; Ra, rapamycin; TA, total cross-sectional heart area; AAR, area at risk; IA, infract area.