RESUMO
AIM: The Shexiang Baoxin pill (SBP) is a commonly used drug for the treatment of coronary artery disease in China. More recently, some studies have found that it improved coronary microvascular function. This study aimed to explore the possible mechanism by which the SBP promotes angiogenesis after acute myocardial infarction (AMI). METHODS: A rabbit model of acute myocardial infarction was established by ligating the left anterior descending coronary artery with silk thread, and the limb lead electrocardiogram was recorded to determine the success of the model. The rabbits were divided into a control group (SBP + normal rabbit group), a sham operation group, a saline + AMI group and an SBP + AMI group. There were 10 rabbits in each group. The animals were sacrificed and myocardial tissue was collected seven days after the operation. Haematoxylin-eosin staining was used to observe the histological changes in the rabbit myocardium in each group. The degree of acute myocardial infarction was observed with picric acid staining, which was used to detect the expression of vascular endothelial growth factor (VEGF), silent information regulator 1 (SIRT1), Beclin1 and mTOR protein in the myocardial tissue of each group. Immunofluorescence CD31-labelled microvascular density (MVD) was used to observe the vascular regeneration of the rabbits in each group. RESULTS: Compared with the normal saline + AMI group, the myocardial infarction area of the SBP + AMI group decreased and CD31 immunofluorescence-labelled MVD increased. Compared with the control and sham operation groups, the expression of VEGF, Beclin1 and mTOR in the normal saline + AMI group and the SBP + AMI group increased, while the expression of SIRT1 decreased. Compared with the normal saline + AMI group and the SBP + AMI group, the positive expression of VEGF, Beclin1, mTOR and SIRT1 in the SBP + AMI group was significantly increased. CONCLUSION: Autophagy was enhanced after acute myocardial infarction. SBP may affect angiogenesis through the SIRT1/mTOR signalling pathway after acute myocardial infarction to inhibit ventricular remodelling and a decline in cardiac function.
