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. 2018 May 15;9:497. doi: 10.3389/fphar.2018.00497

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Copyright © 2018 Wu, Li, Cui, Wu, Hong, Li, Wu, Jie, Wang and Li.

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 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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Schematic illustration showing the main cascade of molecules in cardiomyocytes subjected to ischemia/reperfusion insult and the mechanism of acacetin effects. Cardiomyocytes suffering from hypoxia/reoxygenation induces oxidative stress and triggers ROS production that induces inflammation and apoptosis via releasing the pro-inflammatory cytokines TLR-4 and IL-6 which increase the apoptotic proteins Bax and cleaved caspase-3, and decrease anti-inflammatory factor IL-10 and anti-apoptotic protein Bcl-2. Acacetin activates Nrf2 by stimulating AMPK, and increasing HO-1, SOD1, and SOD2, thereby conferring protection to cardiomyocytes against hypoxia/reoxygenation insult by reducing ROS production and inhibiting inflammation and apoptosis.