Abstract
Huangqi Jianzhong Tang (HQJZT) is a traditional Chinese herbal formula consisting of seven different herbs: Radix Astragali, Radix Paeoniae Alba, Ramulus Cinnamomi, Fructus Jujubae, Glycyrrhizae Radix Et Rhizoma Praeparata Cum Melle, Rhizoma Zingiberis Recens, and Saccharum Granorum. The present study aims to evaluate the possible effects of HQJZT on cardiac function in acute myocardial infarction (AMI) and related mechanism. AMI model was established by ligation of the left anterior descending coronary artery followed by one-week HQJZT treatment. Survival rate was calculated. Rat heart function was assessed by heart performance analysis system. 5-Triphenyltetrazolium chloride (TTC) staining was used to observe myocardial infarct size. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining and western blot were applied to evaluate tissue apoptotic level. Treatment with high dose of HQJZT improved cardiac function, reduced infarct size, number of apoptotic cells and expression of apoptotic proteins, Bax (a proapoptotic protein), and increased expression of antiapoptotic protein, Bcl2. However, enalapril (an angiotensin-converting enzyme inhibitor) treatment did not show marked improvement of these parameters. Our present data suggest that HQJZT has potential therapeutic effects to improve cardiac function by regulation of apoptotic signaling pathway.
Highlights
Heart failure is the terminal stage of cardiovascular disease
acute myocardial infarction (AMI) significantly decreased cardiac function compared with the sham group, by decreasing the diastolic arterial pressure (DAP) and mean arterial pressure (MAP), Pmax, ± dp/dtmax (Table 2)
We clearly demonstrate that Huangqi Jianzhong Tang (HQJZT) improves cardiac function and reduces myocardial infarction injury. e related mechanism may be through regulation of cell apoptosis cascades
Summary
Heart failure is the terminal stage of cardiovascular disease. Most of the myocardial infarction (MI) cases will develop into heart failure. E common consequence of MI is cardiac tissue death induced by heart dysfunction [1, 2]. Primary percutaneous coronary intervention (PPCI) has been developed to restore blood to rescue MI patients; reperfusion paradoxically induces myocardial injury and cardiomyocyte death, thereby mitigating the full benefits of PPCI [3]. Conservative treatment includes the application of antithrombotic drugs, beta-blockers, lipid-lowering drugs, nitrates, calcium antagonists, angiotensin-converting enzyme inhibitors (ACEI), and angiotensin II receptor-1 blockers; the clinical outcome of these treatments is still disappointed [4, 5]. Erefore, exploring novel additional or alternative therapies to satisfy clinical demands is still essentially necessary Conservative treatment includes the application of antithrombotic drugs, beta-blockers, lipid-lowering drugs, nitrates, calcium antagonists, angiotensin-converting enzyme inhibitors (ACEI), and angiotensin II receptor-1 blockers; the clinical outcome of these treatments is still disappointed [4, 5]. erefore, exploring novel additional or alternative therapies to satisfy clinical demands is still essentially necessary
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