Study on the effect of myocardial injury induced by electrical injury in mice based on metabolomics

Objective: To study myocardial injury induced by electrical injury in mice based on metabolomics, and to find out the differential metabolites and pathways in cardiac metabolism omics. Methods: Forty C57BL/6J mice were randomly divided into control group and electric shock group, with 20 mice in each one. The mouse heads in the control group were only stimulated with the sound and light of the electric shock device for 5 s, and those in the electric shock group were continuously shocked with the electric shock device for 5 s. Then the blood of two groups was collected by the method of eyeball blood collection and the serum brain natriuretic peptide (BNP) and myocardial enzyme spectrum were detected. Cardiac tissue was taken by heart perfusion method for paraffin sections and myocardial hematoxylin-eosin (HE) staining, Prussian blue (PB) staining and wheat germ agglutinin (WGA) staining were performed to observe the pathological changes of the myocardium. The cardiac tissue of mice without perfusion was examined by metabolomics. Results: Compared with the control group, the contents of serum BNP and lactate dehydrogenase 1 (LDH1) of mice in the electric shock group were increased (P＜0.05). The WGA staining showed that the mean cell area of cardiomyocytes was increased significantly (1.64±0.23) vs. (1.93±0.14), P＜0.01. Cardiometabolic analysis was performed with the criterion of OPLS-DA VIP＞1 and P＜0.05 for screening differential metabolites. Six up-regulated differential metabolites and 13 upregulated differential metabolites were screened. The results of KEGG pathway enrichment analysis showed that differential metabolites mainly affected cancer-related pathways such as center carbon metabolism in cancer, as well as alanine, aspartic acid and glutamate metabolism. Conclusion: Electrical injury can lead to myocardial injury in mice, mainly manifested as increased serum BNP and LDH1 content, cardiomyocyte hypertrophy and abnormal myocardial metabolic pathway, mainly centered on center carbon metabolism in cancer.