Mulberrin Confers Protection against Doxorubicin-Induced Cardiotoxicity via Regulating AKT Signaling Pathways in Mice

Figure 1

Mulberrin-suppressed DOX-induced ROS generation and oxidative stress in cardiomyocytes. Cell viability (a) and the release of LDH (b) and CK (c) were performed to estimate the toxic effects on cells in response to DOX. The ROS level (d, e), GSH content (f), MDA content (g), and protein carbonyl content (h) in the DOX-treated cells were detect to reflect oxidative damage caused by DOX. Nrf2 and HO-1 protein (i) were detected in the indicated groups. The mRNA levels of Nrf2 downstream gene products (j) were also quantified. Data are presented as . for each group at each time point. compared with the PBS group; ^# compared with DOX alone.

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