A study on the molecular mechanism of Baicalin in improving Myocardial Fibrosis based on network pharmacology and experimental verification

This study aimed to evaluate the pharmacological mechanism of baicalin intervention on myocardial fibrosis through network pharmacological analysis, molecular docking, and experimental verification.The chemical components and targets of all the drugs in the Baicalin were obtained through Target Prediction databases. The targets of Myocardial fibrosis(MF)were screened through the GeneCards and OMIM databases. The obtained targets were imported into Cytoscape 3.9 software to construct the active ingredient target network and were imported into the String database to construct PPI network, and the in Cytoscape 3.9 was used for network topology analysis. Gene Ontology (GO) enrichment analysis and Kyoto gene and genomic (KEGG) enrichment analysis were performed on the potential targets of Wuling decoction for MF using the David database.The results were imported into bioinformatics platform to obtain GO and KEGG network relationship maps. The molecular docking software AutoDock Vina was used to dock the core targets with the active ingredients. A MF rat model was established and animals were divided into the control, MF model, a captopril group (9 mg/kg), and low-, middle-, and high-dose baicalin groups (50, 100, 200 mg/kg). Compared with the rats in the MF model group, rats in each administration group demonstrated restoration of ST segment amplitude and T wave on electrocardiograms. Moreover, HWI and LVWI exhibited significant decreases. The levels of CK, LDH, NT-proBNP, Col I and Col III in myocardial tissue also showed significant decreases. Additionally,the degree of myocardial fibrosis was reduced; there were also significant decreases observed in the expression levels of PTGS2 and TNF-α in myocardial tissue, where as an increase was noted in the expression level of IL2. Baicalin has been shown to enhance myocardial fibrosis and cardiac function in a rat model of myocardial fibrosis. The mechanism underlying this effect appears to be associated with the down-regulation of PTGS2 and TNF-αexpression levels, as well as the up-regulation of IL2 expression levels.