Research Paper Volume 11, Issue 22 pp 10061—10073
PGC1α activation by pterostilbene ameliorates acute doxorubicin cardiotoxicity by reducing oxidative stress via enhancing AMPK and SIRT1 cascades
Figure 6. Schematic diagram summarizing the myocardial protective actions of pterostilbene against acute DOX cardiotoxicity via the PGC1α activation through stimulating AMPK and SIRT1 cascades. Pterostilbene treatment enhances the AMPK phosphorylation and SIRT1 upregulation thus increasing the PGC1α expression and inhibiting PGC1α acetylation. These effects markedly increase the levels of UCP2 and NRF1, and inhibits oxidative stress via decreasing ROS generation and increasing ATP content, SOD2 and GPx activities in cardiomyocytes.