BackgroundThis study identified microRNAs (miRNAs) and mRNAs associated with Compound Longmaining (CLMN) treatment of acute myocardial infarction (AMI). Our results provide a theoretical framework to guide AMI treatment and improve myocardial injury.Material/MethodsThe myocardial tissues of the sham operation group (S), the model group (M), and the CLMN treatment group (T) were obtained. The mRNA and miRNA expression profiles were identified using RNA-sequencing analysis. The sequencing results were verified by quantitative real-time PCR (qRT-PCR). Bioinformatics was used to predict the function of differentially expressed genes (DEGs) and related signal transduction pathways. The target genes of miRNAs were predicted by software analysis, and the relationship between miRNA and mRNA was studied by network analysis.ResultsRNA-sequencing revealed 22 differentially expressed miRNAs (DEMs) and 76 DEGs in myocardial tissue. Six DEMs and 9 DEGs were randomly selected for qRT-PCR validation, and corroborating results were obtained. The results of Gene ontology (GO) showed that DEGs participated in different biological processes. Through the combined analysis of miRNAs and mRNAs expression, it was confirmed that a single miRNA is involved in the regulation of multiple genes, and also multiple miRNAs can target one gene.ConclusionsThe analysis based on the miRNA-mRNA network can not only help to elucidate the potential molecular mechanism of CLMN treatment of AMI, but can also help in identifying novel therapeutic targets.
Background and objective: Myocardial Infarction (MI) is a cardiovascular disease with a high morbidity and mortality rate. While MI is currently treated with pharmaceuticals, there is a need for new treatment options: compound Chinese medicines may have unique advantages for the treatment of MI. In this study, we used network pharmacology to explore the molecular mechanisms of action of Chinese Longmai Ning decoction (CLMN) as a potential treatment approach.Methods: Chip data related to Myocardial Infarction were downloaded from the GEO database and genes from GSE48060 and GSE66360 chips were obtained by R language. The targets of active components of compound CLMN and myocardial infarction disease were predicted by network pharmacology. After intersection analysis, the core targets were obtained and functional enrichment analysis was carried out. CLMN biological activity was verified by molecular docking prior to establishing a mouse MI model to verify efficacy using hematoxylin-eosin staining (HE) and immunohistochemistry.Results: KEGG pathway analysis showed that TNF, IL1B, PTGS2, VCAM1, and NFKBIA which mainly act on NF-kappa B pathway contribute to the anti-inflammatory effects of CLMN. Immunohistochemical analysis showed that TNF-α and TRAF-2 expression levels in MI of CLMN-treated mice were decreased, while IkBα was increased (P < 0.05). HE staining showed CLMN reduced inflammation in mouse cardiomyocytes and decreased fibrosis.Conclusion: CLMN regulates the NF-kappa B signaling pathway and the expression of TNF, IL1B, PTGS2, VCAM1 and NFKBIA. Chemical analysis showed that CLMN active components such as Daidzein-4,7-diglucoside, rutin and puerarin may be responsible for the therapeutic effect of the decoction.
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