morroniside and Myocardial-Infarction

Angiogenesis is critical for re-establishing blood supply to the ischemic myocardium after acute myocardial infarction (AMI). This study aimed to investigate the effects of morroniside on angiogenesis after AMI and explored associated proangiogenic mechanisms. A rat model of AMI was established by ligation of the left anterior descending coronary artery followed by administration of three doses of morroniside. Immunofluorescence staining was performed to identify newly generated endothelial cells and arterioles. The protein expression levels associated with angiogenesis were examined by western blots. Echocardiography was used to examine cardiac function. Our data revealed that morroniside promoted angiogenesis and improved cardiac function in rats with AMI. The proangiogenic effect of morroniside might be mediated by the VEGFA/VEGF receptor 2 signaling pathway.

Topics: Administration, Oral; Animals; Coronary Vessels; Disease Models, Animal; Glycosides; Humans; Male; Myocardial Infarction; Myocardium; Neovascularization, Physiologic; Rats; Signal Transduction; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2

The aim of this study is to investigate the cardioprotective effects of morroniside in rats following acute myocardial infarction. An acute myocardial infarction (AMI) was induced by ligating the anterior descending coronary artery (LAD) [1]. Following AMI, morroniside was administered intragastrically for 24 h at doses of 45, 90, and 180 mg/kg, respectively. Biomarkers such as creatine kinase (CK-MB), lactate dehydrogenase (LDH), ɑ-hydroxybutyrate dehydrogenase (ɑ-HBDH), and aspartate aminotransferase (AST) activities in AMI rats in the serum were detected with commercial kits [2]. Following AMI, morroniside was administered intragastrically for 72 h at doses of 45, 90, and 180 mg/kg/d, respectively. The expression of nuclear factor kappa B (NF-κB) in cardiac myocardium was detected by western blotting analysis. Meanwhile, cardiac function was measured by echocardiography. We observed morroniside decreased the levels of CK-MB, LDH, ɑ-HBDH, and AST activities in AMI rats after 24 h. We also found that morroniside reduced the expression of NF-κB in cardiac myocardium at 72 h post AMI rats. Further, cardiac function was improved by administration of morroniside. Collectively, our findings demonstrated that morroniside had cardioprotective effects in rats following acute myocardial infarction. Attenuation of inflammation might contribute to the cardioprotective effects of morroniside.

Topics: Animals; Biomarkers; Cardiotonic Agents; Echocardiography; Glycosides; Myocardial Infarction; NF-kappa B; Rats; Time Factors; Treatment Outcome