Abstract
Myocardial infarction can lead to ventricular remodeling and arrhythmia, which is closely related to nerve remodeling. Our previous study found that Yiqi Huoxue decoction (YQHX) can improve ventricular remodeling and reduce myocardial damage. Therefore, in this study, we observed the effect of YQHX on cardiac neural remodeling and cardiomyocyte hypertrophy and its possible mechanism. This research is composed of two parts: animal and H9c2 cells experiments. The animal model of acute myocardial infarction was established by ligating the left anterior descending coronary artery in Sprague Dawley (SD) rats. H9c2 cells were placed in 94% N2, 5% CO2, and 1% O2 hypoxic environment for 12 hours to replicate the hypoglycemic hypoxia model. The experimental results showed that, compared with the MI group, YQHX can significantly improve heart function after myocardial infarction and reduce nerve remodeling and myocardial hypertrophy. Pathological structure observation demonstrated reducing myocardial tissue damage and decreasing of cell cross-sectional area, diameter, and circumference. The positive rate of TH declined apparently, and the sympathetic nerve density was lower than that of the MI group. After YQHX was given for 28 days, the proneural remodeling factors TH, NGF, and GAP43 in the marginal zone of infarction and stellate ganglion decreased obviously while the inhibitory nerve remodeling factor Sema-3A increased. The myocardial hypertrophic protein ANP and β-MHC were also significantly inhibited with p-ERK1/2 protein expression level prominently reduced. There was no difference between the YQHX group and the Meto group. After myocardial infarction, nerve remodeling was seen in the marginal area of infarction and stellate ganglion, and the neuropeptides released by which promoted myocardial hypertrophy. The mechanism may be related to the ERK1/2 signaling pathway. YQHX could regulate the ERK1/2 signaling pathway, inhibit the release of nerve remodeling factors and myocardial hypertrophy protein to reduce nerve remodeling, and relieve myocardial hypertrophy.
Highlights
In cardiovascular diseases, especially ischemic heart disease, abnormal autonomic nerve regulation plays a vital role in the occurrence, development, and prognosis of the disease [1, 2]
Compared with the sham operation group (Sham) group, the myocardial cells of Myocardial infarction (MI) group arranged disorderly and the quantity decreased. e cell morphology was abnormal with scattering nuclei, a large number of inflammatory cells infiltrating with enlarged intercellular space
As a β-blocker, metoprolol has sufficient evidencebased medical evidence to verify that it can block or delay myocardial remodeling and improve long-term prognosis [35, 36]. e effects of Yiqi Huoxue decoction (YQHX) and metoprolol on cardiac function after myocardial infarction were observed. e results showed that taking YQHX for 28 days can significantly improve the ejection fraction (EF), FS, left ventricular end systolic diameter (LVIDs), and left ventricular end diastolic diameter (LVIDd) of rats after myocardial infarction and improve the pathological structure of the infarct marginal area tissue. ere is no significant difference between YQHX and metoprolol, but its efficacy is superior to metoprolol in the chronic phase
Summary
Especially ischemic heart disease, abnormal autonomic nerve regulation plays a vital role in the occurrence, development, and prognosis of the disease [1, 2]. Myocardial infarction (MI) can lead to ventricular remodeling, arrhythmia, and sudden death. It is an important cause of death, which is closely related to nerve remodeling [3, 4]. Evidence-Based Complementary and Alternative Medicine mechanisms at the early stage after MI, but the long-term activation at a high level of the sympathetic nervous system is an important facilitator in the occurrence of ventricular remodeling and deterioration of the disease due to its adverse effect on the heart itself and cardiac function [7]. Neural remodeling factors play a very important role in this process, reflecting the activity of sympathetic nerves [10], promoting the repair of sympathetic nerve damage [11], and avoiding excessive growth [12]. Neural remodeling factors play a very important role in this process, reflecting the activity of sympathetic nerves [10], promoting the repair of sympathetic nerve damage [11], and avoiding excessive growth [12]. e hyperproliferation of sympathetic nerve endings will release a large amount of catecholamines and neuropeptides (NE, NPY), which can promote cardiac hypertrophy and ventricular hypertrophy, leading to heart failure and sudden death
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