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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 Compound Longmaining (CLMN) decoction 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 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 (HE) staining 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. |
