Background
Baicalin is a generally available flavonoid with potent biological activity. The present study aimed to assess the underlying mechanism of baicalin in treatment of atherosclerosis (AS) with the help of network pharmacology, molecular docking and experimental validation.
Conclusion
Collectively, we combined network pharmacology and endothelial injury models to investigate the anti-AS mechanism of baicalin. The results demonstrate that baicalin may exert anti-oxidative stress effects by targeting NOX4, providing new mechanisms and insights to baicalin for the treatment of AS.
Methods
The target genes of baicalin and AS were identified from public databases, and the overlapping
Results
In this study, baicalin had 45 biological targets against AS. Functional enrichment analysis demonstrated that most targets were involved in oxidative stress. Using the CytoHubba plug-in, we obtained the top 10 genes in the PPI network ranked by the EPC algorithm. Molecular docking and microarray dataset validation indicated that NOX4 may be an essential target of baicalin, and its expression was significantly suppressed in AS samples compared to controls. In endothelial injury model, intervention of HAECs with baicalin increased the expression levels of NOX4 and NOS3 (eNOS), and decreased LPS-induced ROS generation. After inhibition of NOX4, the anti-ROS-generating effect of baicalin was abolished.