Key result
Puerarin at 120 mg/kg and 60 mg/kg significantly reduced infarct area and induced angiogenesis in both ischemic and non-ischemic myocardium of rats following myocardial infarction.
Why the study?
Does puerarin reduce infarct size and induce angiogenesis in a rat model of myocardial infarction?
Does puerarin reduce infarct size and induce angiogenesis in a rat model of myocardial infarction?
In a rat model of myocardial infarction, puerarin reduced infarct size and promoted angiogenesis, potentially via upregulation of VEGF and eNOS.
Puerarin attenuates post-MI remodeling in rats; leaves open translation to human therapy pending clinical trials.
Puerarin is a major effective ingredient extracted from the traditional Chinese medicine ge-gen (radix puerariae, RP). Recently, puerarin has been used to treat patients with coronary artery diseases (CAD). However, the mechanisms of puerarin on coronary artery diseases are still not very clear. In this study, we investigated the role of puerarin on angiogenesis in the non-ischemic and ischemic myocardium. We found that puerarin (120, 60 mg/kg, i.p.) could reduce infarct area in the heart of rat with myocardial infarction (MI). Puerarin (120 mg/kg) induced angiogenesis in the non-ischemic and ischemic myocardium, which was one of the mechanisms of curing coronary artery diseases. The gene expression or activation of vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1alpha (HIF-1alpha) and endothelial nitric oxide synthase (eNOS) that correlated with angiogenesis were also induced by puerarin. From these results, we suggested that puerarin may induce therapeutic angiogenesis in myocardium of rat with MI. The mechanism may be that puerarin can induce VEGF and eNOS expression.
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Zhang et al. (2006) studied Myocardial infarction (n=88). Puerarin vs. No treatment (model group) was evaluated on Infarct size as a percentage of total myocardium area (p=<0.05). Puerarin at 120 mg/kg and 60 mg/kg significantly reduced infarct area and induced angiogenesis in both ischemic and non-ischemic myocardium of rats following myocardial infarction.
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