Abstract
Chronic alcohol consumption leads to myocardial injury, ventricle dilation, and cardiac dysfunction, which is defined as alcoholic cardiomyopathy (ACM). To explore the induced myocardial injury and underlying mechanism of ACM, the Liber-DeCarli liquid diet was used to establish an animal model of ACM and histopathology, echocardiography, molecular biology, and metabolomics were employed. Hematoxylin-eosin and Masson’s trichrome staining revealed disordered myocardial structure and local fibrosis in the ACM group. Echocardiography revealed thinning wall and dilation of the left ventricle and decreased cardiac function in the ACM group, with increased serum levels of brain natriuretic peptide (BNP) and expression of myocardial BNP mRNA measured through enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction (PCR), respectively. Through metabolomic analysis of myocardium specimens, 297 differentially expressed metabolites were identified which were involved in KEGG pathways related to the biosynthesis of unsaturated fatty acids, vitamin digestion and absorption, oxidative phosphorylation, pentose phosphate, and purine and pyrimidine metabolism. The present study demonstrated chronic alcohol consumption caused disordered cardiomyocyte structure, thinning and dilation of the left ventricle, and decreased cardiac function. Metabolomic analysis of myocardium specimens and KEGG enrichment analysis further demonstrated that several differentially expressed metabolites and pathways were involved in the ACM group, which suggests potential causes of myocardial injury due to chronic alcohol exposure and provides insight for further research elucidating the underlying mechanisms of ACM.
Highlights
With the development of the social economy, increased alcohol consumption has led to serious problems worldwide [1]
Individual differences in different batches of animals may lead to the discrepancies in some of the parameters of echocardiography, serum brain natriuretic peptide (BNP) levels, and BNP mRNA of myocardium compared to our previous report [1]
Despite all this, based on the results of echocardiography, histology, serum BNP levels, and BNP mRNA in myocardium, we can conclude that the Alcoholic cardiomyopathy (ACM) model was successfully established in the present study, which is the basis for further myocardial metabolomics study
Summary
With the development of the social economy, increased alcohol consumption has led to serious problems worldwide [1]. Alcoholic cardiomyopathy (ACM), the most common form of myocardial injury caused by chronic alcohol consumption, manifests as a progressive decrease in myocardial contractility and ventricular dilatation, leading to heart failure and arrhythmia [2]. Metabolomics is a new method of studying biological systems developed after genomics and proteomics. By analyzing small molecular substances in biological fluids and tissues, metabolomics reveals metabolic patterns and provides insight into the mechanisms underlying physiological conditions and diseases [5]. There are currently no metabolomic reports on myocardial injury due to chronic alcohol consumption. The present study employed histopathology, echocardiography, molecular biology, and metabolomics to explore the myocardial injury induced by chronic alcohol consumption and the underlying mechanism of ACM
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