RESUMEN
<b>Objective::To study the protective effect and mechanism of Qidong Yixin oral liquid on doxorubicin-induced myocardial toxicity in mice. <b>Method::Ninety male ICR mice were randomly divided into normal group, model(DOX) group, DOX+ Qidong Yixin oral liquid group (9.55, 23.88, 47.75 g·kg<sup>-1</sup>) and high dose group (47.75 g·kg<sup>-1</sup>) with 15 mice in each group. The normal group and model group were given pure water by gavage, and each dose group of Qidong Yixin oral liquid was given different doses of Qidong Yixin oral liquid once a day for 21 days. On the seventh day, normal saline was injected into the abdominal cavity of the normal group and the high dose group of Qidong Yixin oral liquid. Doxorubicin was injected into the abdominal cavity of the other groups (15 mg·kg<sup>-1</sup>). After 21 days, the weight and heart weight of mice were weighed and cardiac index was calculated. Serum was taken for the detection of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST). Heart was taken for hematoxylin-eosin (HE) staining, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (CAT) in myocardial tissue were detected. The expression of nuclear factor NF-E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot. <b>Result::Compared with normal group, adriamycin could significantly reduce the body weight of mice (<italic>P</italic><0.01), increase the activities of LDH, CK and AST in serum(<italic>P</italic><0.01), and decrease the activities of antioxidant enzymes (<italic>P</italic><0.01). Compared with DOX group, high dose Qidong Yixin oral liquid could significantly increase the weight of mice (<italic>P</italic><0.05, <italic>P</italic><0.01), decrease the level of myocardial three enzymes(<italic>P</italic><0.01), increase the activity of antioxidant enzymes(<italic>P</italic><0.05, <italic>P</italic><0.01), and increase the expression of Nrf2 and HO-1(<italic>P</italic><0.01). <b>Conclusion::Qidong Yixin oral liquid has a good protective effect on doxorubicin myocardial toxicity. Its mechanism may be related to activating Nrf2/HO-1 signaling pathway and alleviating oxidative stress injury.