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

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Figure 1. Effect of pterostilbene treatment on cell viability, mitochondrial membrane potential, ROS generation, mitochondrial morphologic changes in DOX-treated H9c2 cells (24 h). (A) single pterostilbene (2.5-10 μM) treatment and cotreatment of 1 μM DOX with increasing concentrations of pterostilbene (2.5-10 μM) on H9c2 cell viability (24 h). (B) mitochondrial membrane potential (ΔΨm) was expressed as the ratio of JC-1 polymer/monomer; red fluorescence represents the mitochondrial JC-1 polymer, and green fluorescence represents the monomeric form of JC-1, indicating ΔΨm depolarization. (C) Representative images and ROS level, and the indexes in the control group are defined as 100%. (D) Representative images of the ultrastructural morphology of mitochondria in each group of H9c2 cells are shown. The results are expressed as the mean ± SEM. *P < 0.05 vs. the control group, #P < 0.05 vs. the 1 μM DOX-treated group.