Abstract: AIM: To explore the protection of Hyperoside (Hyp) on heart and thoracic aorta in mice with myocardial infarction (MI) as well as its potential mechanism.  METHODS: The MI model was generated by a ligation on the left anterior descending coronary artery. The mice were then randomly divided into sham group (saline, 0.1 mg/10 g), model group (saline, 0.1 mg/10 g), Hyp-low, moderate and high concentration groups (Hyp, 9, 18 and 36 mg/kg), Fosinopril group (Fosinopril, 15 mg/kg), and Hyp-high concentration + 3-MA group (Hyp, 36 mg/kg; 3-MA, 30 mg/kg). The mice were treated with Hyp and Fosinopril for two weeks, and then the changes of heart weight versus body weight (HW/BW), electrocardiogram (ECG) remodeling, cardiac function, oxidative stress level in serum, thoracic aorta remodeling and endothelial function were investigated. RESULTS: In the model group, the HW/BW was elevated (P<0.01). The width of QRS in ECG was elevated, as a company with the reduction of height of QRS (P<0.01). The echocardiography assay showed that the cardiac cavity was enlarged (P<0.01). The oxidative stress level in serum was enhanced (P<0.01). The thoracic aorta remodeling and endothelial dysfunction became more serious (P<0.01). After being treated with different concentrations of Hyp and fosinopril for two weeks, the changes above were reserved (P<0.05, P<0.01). Co-treatment with 3-MA, an autophagy inhibitor, suppressed the protective effects of Hyp on impaired hearts and vessels (P<0.05, P<0.01). CONCLUSION: Hyp has protective prospects on injured heart and thoracic aorta remodeling, as well as endothelial dysfunction in MI mice; 3-MA, an autophagy inhibitor, can reverse the cardiovascular protection of Hyp. The mechanism may be explained that Hyp can elevate autophagy level in heart, which further weaken oxidative injury in MI mice.

Key words: myocardial infarction, hyperoside, thoracic aorta, autophagy