Myricitrin Protects against Doxorubicin-Induced Cardiotoxicity by Counteracting Oxidative Stress and Inhibiting Mitochondrial Apoptosis via ERK/P53 Pathway

Figure 3

Effects of myricitrin on Dox-induced cardiotoxicity in vitro. The H9c2 cells were treated with various concentrations of myricitrin (3.125, 6.25, 12.5, and 25 μg/mL) for 12 h, and the cell viability was determined using the CCK8 assay and expressed as the percentage relative to the control group (a). The control and myricitrin-treated cells were subsequently exposed to 1 μM Dox for an additional 36 h, and the cell viability (b) and LDH release were measured (c). All data are expressed as the means ± SD (). versus Cont; versus Dox.

(a)

(b)

(c)