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

<div>Involvement of ERK1/2 phosphorylation in myricitrin-mediated expression of p53, Bcl-2, and Bax. H9c2 cardiomyocytes were pretreated with or without myricitrin (25 <i>μ</i>g/mL) for 12 h prior to Dox exposure. Effects of SP600125 (a JNK-specific inhibitor) and PD98059 (an ERK-specific inhibitor) on myricitrin-mediated activation of p53 were measured by immunoblotting assay (a). Effects of PD98059 (an ERK-specific inhibitor) and PFT-<i>α</i> (an p53-specific inhibitor) on the expression of Bcl-2 and Bax were measured by immunoblotting assay (b).</div>

Evidence-Based Complementary and Alternative Medicine

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Figure 9

Figure 9: Myricitrin Protects against Doxorubicin-Induced Cardiotoxicity by Counteracting Oxidative Stress and Inhibiting Mitochondrial Apoptosis via ERK/P53 Pathway 

Figure 9 | Myricitrin Protects against Doxorubicin-Induced Cardiotoxicity by Counteracting Oxidative Stress and Inhibiting Mitochondrial Apoptosis via ERK/P53 Pathway 