Abstract

Glutathione is an important antioxidant that plays an important role in myocardial remodeling. However, the exact mechanisms underlying the effects of glutathione on heart failure are elusive. This study aimed to investigate the mechanisms of glutathione in heart failure treatment based on network pharmacology technology. The gene expression profiles were downloaded from Gene Expression Omnibus database (GSE133054). Differentially expressed genes were identified by Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis. A protein protein interaction network was constructed to screen potential regulatory proteins. We identified 970 potential target genes of glutathione and 2381 differentially expressed genes of heart failure, with 80 genes overlapping in both groups. Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the important genes were mainly distributed in phosphatidylinositol 3 kinase-protein kinase B signaling pathway, mitogen-activated protein kinase signaling pathway, lipid and atherosclerosis pathway. In glutathione target genes-heart failure network analysis, 7 targets were identified, including tumor necrosis factor, vascular endothelial growth factor A, fibronectin 1, serine proteinase inhibitor 1, insulin-like growth factor binding protein 3, matrix metalloproteinase-1 and liquid oxygen, with serine proteinase inhibitor 1, insulin-like growth factor binding protein 3, fibronectin 1 and liquid oxygen significantly over expressed in heart failure. We utilized network pharmacology to systematically explore the mechanism of action of glutathione on heart failure and identified genes and pathways as potential therapeutic targets for heart failure.