Angiogenic function of astragaloside IV in rats with myocardial infarction occurs via the PKD1-HDAC5-VEGF pathway

The current study aimed to assess the role and mechanism of astragaloside IV (AS-IV) in myocardial infarction. A myocardial infarction model was established via the ligation of the left anterior descending artery. Rats were randomly divided into sham, DMSO, model, AS-IV, AS-IV-CID755673 and CID755673 inhibitor groups. Rats were then sacrificed following 4 weeks of treatment and segmental heart samples were obtained for hematoxylin and eosin, and masson staining. The expression of PKD1, HDAC5 and VEGF were analyzed using immunohistochemistry, reverse transcription polymerase chain reaction and western blotting. Compared with the sham and DMSO groups, the morphology of myocardium in the model and CID755673 inhibitor groups were disordered and exhibited necrotic myocardial cells and collagen tissues. Following treatment with AS-IV, the morphology of the myocardium was markedly improved and the number of new blood vessels increased. However, following treatment with CID755673, the myocardial tissue of rats became disordered, with an increased number of necrotic cells and the closure of certain vessels. The expression of PKD1, HDAC5 and VEGF mRNA and protein in myocardial tissue of model group and CID755673 inhibitor group were significantly lower than the other four groups (P<0.05), whereas these levels in the AS-IV group were significantly higher than those in the other five groups (P<0.01). Additionally, the AS-IV-CID755673 group exhibited significantly higher levels of PKD1, HDAC5 and VEGF mRNA and protein than the sham, DMSO, CID755673 inhibitor and model groups (P<0.05). Furthermore, the protein expression of pS205 PKD1, pS259 HDAC5 and pTyr951 VEGF in the myocardium of rats was comparable with that of PKD1, HDAC5 and VEGF. AS-IV may partly promote the angiogenesis of myocardial tissue in rats with myocardial infarction via the PKD1-HDAC5-VEGF pathway.