Abstract
Background Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. The idea of therapeutic angiogenesis in ischemic myocardium is a promising strategy for MI patients. Buyang Huanwu decoction (BHD), a famous Chinese herbal prescription, exerted antioxidant, antiapoptotic, and anti-inflammatory effects, which contribute to cardio-/cerebral protection. Here, we aim to investigate the effects of BHD on angiogenesis through the caveolin-1 (Cav-1)/vascular endothelial growth factor (VEGF) pathway in MI model of mice. Materials and Methods C57BL/6 mice were randomly divided into 3 groups by the table of random number: (1) sham-operated group (sham, n = 15), (2) AMI group (AMI+sham, n = 20), and (3) BHD-treated group (AMI+BHD, n = 20). 2,3,5-Triphenyltetrazolium chloride solution stain was used to determine myocardial infarct size. Myocardial histopathology was tested using Masson staining and hematoxylin-eosin staining. CD31 immunofluorescence staining was used to analyze the angiogenesis in the infarction border zone. Western blot analysis, immunofluorescence staining, and/or real-time quantitative reverse transcription polymerase chain reaction was applied to test the expression of Cav-1, VEGF, vascular endothelial growth factor receptor 2 (VEGFR2), and/or phosphorylated extracellular signal-regulated kinase (p-ERK). All statistical analyses were performed using the SPSS 20.0 software and GraphPad Prism 6.05. Values of P < 0.05 were considered as statistically significant. Results and Conclusion Compared with the AMI group, the BHD-treated group showed a significant improvement in the heart weight/body weight ratio, echocardiography images, cardiac function, infarct size, Mason staining of the collagen deposition area, and density of microvessel in the infarction border zone (P < 0.05). Compared with the AMI group, BHD promoted the expression of Cav-1, VEGF, VEGFR2, and p-ERK in the infarction border zone after AMI. BHD could exert cardioprotective effects on the mouse model with AMI through targeting angiogenesis via Cav-1/VEGF signaling pathway.
Highlights
Based on the fourth edition of universal definition of myocardial infarction (MI), acute MI (AMI) was defined as having clinical evidences of acute myocardial injury with at least one of the following items: clinical symptoms of myocardial ischemia, new ischemic changes in electrocardiogram (ECG), development of pathological Q waves, imaging evidences in accordance with an ischemic aetiology as new loss of surviving myocardium or new regional ventricular wall motion abnormality, and identification of a coronary thrombus by coronary angiography or autopsy [1]
The process of restoring coronary blood flow to the ischemic myocardium may lead to myocardial ischemia/reperfusion (I/R) injury such as myocardial stunning, no-reflow phenomenon, and reperfusion arrhythmias
In the present study, we aim to investigate the effects of Buyang Huanwu decoction (BHD) on angiogenesis through the Cav-1/vascular endothelial growth factor (VEGF) pathway on the MI model of mice
Summary
Based on the fourth edition of universal definition of myocardial infarction (MI), acute MI (AMI) was defined as having clinical evidences of acute myocardial injury with at least one of the following items: clinical symptoms of myocardial ischemia, new ischemic changes in electrocardiogram (ECG), development of pathological Q waves, imaging evidences in accordance with an ischemic aetiology as new loss of surviving myocardium or new regional ventricular wall motion abnormality, and identification of a coronary thrombus by coronary angiography or autopsy [1]. The process of restoring coronary blood flow to the ischemic myocardium may lead to myocardial ischemia/reperfusion (I/R) injury such as myocardial stunning, no-reflow phenomenon, and reperfusion arrhythmias. Several strategies such as pharmacological treatment and mechanical therapies could reduce I/R injury in animal studies or small-scale clinical trials, but the results are inconclusive [4]. We aim to investigate the effects of BHD on angiogenesis through the caveolin-1 (Cav1)/vascular endothelial growth factor (VEGF) pathway in MI model of mice. BHD could exert cardioprotective effects on the mouse model with AMI through targeting angiogenesis via Cav-1/VEGF signaling pathway
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