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 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.