Buyang Huanwu Decoction Exerts Cardioprotective Effects through Targeting Angiogenesis via Caveolin-1VEGF Signaling Pathway in Mice with Acute Myocardial Infarction

Abstract EN

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.