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

Figure 2

Effects of myricitrin on the Dox-induced cardiotoxicity in vivo. The rats were intraperitoneally (i.p.) treated with Dox (3 mg/kg every other day for a cumulative dose of 9 mg/kg) in presence or absence of myricitrin (2.5 and 5 mg/kg i.p. before Dox administration). After 28 days, the relative heart weight index (heart weight/body weight ratio g/g) was measured (a). The effects of myricitrin on the LDH (b), CK (c), and AST (d) levels were measured according to the kit manufacturer’s instructions. The effects of myricitrin on the histological changes in the heart tissues were evaluated using HE staining. Solid arrow indicated the abnormal phenotypes including disorganization of myofibrillar arrays, cytoplasmic vacuolization, and intense infiltration with neutrophil granulocytes. Scale bar: 500 µm (e). The values ( per group) are expressed as the means ± SD. versus Cont; and versus Dox.

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