Abstract Background Prunella vulgaris L. (PVL) extracts have been reported to inhibit the proliferation and promote the apoptosis of lung ca
Abstract Background Prunella vulgaris L. (PVL) extracts have been reported to inhibit the proliferation and promote the apoptosis of lung cancer cells. However, its pharmacological mechanism remains unclear. The objective of this study was to explore the main active ingredients and potential molecular mechanisms of PVL in the treatment of non-small cell lung cancer (NSCLC). Materials and methods The differentially expressed genes (DEGs) associated with NSCLC were obtained by analyzing microarray dataset GSE136043 in Gene Expression Omnibus. The bioactive components of PVL were obtained using TCMSP database, and the related targets of PVL were collected using the Swiss Target Prediction database, and drug-disease common targets were subsequently obtained. Protein–protein interaction (PPI) network was constructed using a STRING database and core targets were obtained via Cytoscape 3.9.0 software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the common targets were performed using DAVID database. Molecular docking analysis was then performed using AutoDock Vina software. Finally, the therapeutic activity of morin, a crucial component of PVL, against NSCLC was verified by in vitro experiments. Results A total of 11 active components and 180 targets of PVL were obtained, 39 of which overlapped with NSCLC’s disease targets, and were considered to be “drug-disease” common targets. Morin, luteolin, delphinidin, kaempferol and quercetin were considered key components of PVL in NSCLC treatment. AKT1, MMP9, ESR1, XDH, MAPT, and CYP1B1 were considered to be the core targets in the PPI network. These “drug-disease” common targets were associated with 100 GO items, including 41 biological processes, 16 cellular components, and 43 molecular functions. KEGG enrichment analysis identified 14 signaling pathways. The key components morin, luteolin, delphinidin, kaempferol and quercetin had good binding affinity with the core targets (AKT1, MMP9, ESR1, XDH and CYP1B1). Additionally, morin could inhibit NSCLC cell viability and promote cell apoptosis in a dose-dependent manner. In addition, morin could also reduce mRNA expression levels of core targets. Conclusion PVL may have the potential to treat NSCLC with a multi-component, multi-target and multi-pathway manner.
