摘要Objective: To explore the molecular biological mechanism of the "salvia chinensis and radix ranunculi ternati" drug pair in the treatment of lung cancer based on network pharmacology. Methods: Searching the TCMSP database and previous literatures to screen the active compounds which resist lung cancer activity in salvia chinensis and radix ranunculi ternati. The candidate compounds were unified in the DrugBank to find the corresponding drug targets which were corrected to the standard gene names by the UniProt database. The SwissTargetPrediction platform was used to predict other targets. Searching GeneCards, OMIM and DrugBank to obtain genes related to lung cancer. After taking the intersection, the candidate gene target of drug pair in the treatment of lung cancer could be obtained. The "herbs-compounds-targets-disease" network was bulit with Cytoscape, and the PPI network was bulit on the STRING platform while the core network nodes were screened. GO and KEGG analysis on candidate genes was implemented through Metacape platform, and a "pathways-targets" network was bulit to further screen key genes. Results: A total of 16 active compounds in salvia chinensis, 18 active compounds in radix ranunculi ternati, 164 candidate targets, 2443 GO functions and 170 KEGG pathways was obtained. Conclusion: The effective compounds of " salvia chinensis and radix ranunculi ternati " drug pair in the treatment of lung cancer are quercetin, ursolic acid, β-sitosterol and caffeic acid. The key targets are MAPK1, AKT1, PIK3R1, RAF1 and EGFR. GO functions mainly include cytokines, oxidative stress, plasma membrane transmission, protein kinase binding and activity, apoptosis. KEGG could directly regulate pathways in cancer, non-small cells lung cancer pathway and small cell lung cancer pathway. KEGG also involves EGFR tyrosine kinase inhibitor resistance, IL-17, TNF, PI3K-AKT signaling pathway and apoptosis. This study reveals the molecular biological mechanism of "salvia chinensis and radix ranunculi ternati" drug pair in the treatment of lung cancer. It is reasoned that its potential targets affect multiple signaling pathways and ultimately resist the proliferation, differentiation, invasion, metastasis and promote apoptosis of lung cancer cells. Evidence for further experimental study is provided by this study.