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

Figure 7

Involvement of ERK1/2 and JNK phosphorylation in myricitrin-mediated inhibition of caspase-3 activation and cytotoxicity. The H9c2 cardiomyocytes were pretreated with or without myricitrin (25 μg/mL) for 12 h prior to Dox exposure. The phosphorylation of ERK1/2 and JNK was detected using immunoblotting (a). The effects of SP600125 (a JNK-specific inhibitor) and PD98059 (an ERK-specific inhibitor) on the myricitrin-mediated inhibition of cleaved caspase-3 production and cytotoxicity in H9c2 cardiomyocytes were measured ((b), (c), and (d)). All data are expressed as the means ± SD (). versus Cont; versus Dox.

(a)

(b)

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(d)