Integrating GEO Database and Bioinformatics Analysis to Screen the Key Targets of Tanshinone IIA in Myocardial Infarction

Objective: To systematically screen the core targets of Tanshinone IIA in the treatment of myocardial infarction (MI) and to explore its molecular mechanisms based on the Gene Expression Omnibus (GEO) database and bioinformatics methods. Methods: MI-related transcriptome datasets (GSE62646, GSE83500) were obtained from the GEO database. The "sva" package was used to correct batch effects, and the "limma" package was employed to identify differentially expressed genes (DEGs). Potential targets of Tanshinone IIA were retrieved by integrating the TCMSP, CTD, and SwissTargetPrediction databases. Intersecting genes were extracted via Venn diagrams, and a protein-protein interaction (PPI) network was constructed. Functional enrichment analysis, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, was performed using DAVID. Molecular docking was conducted using CB-Dock2 to validate binding affinity. Results: A total of 8 core candidate targets were identified, including SCN9A, PIM1, GSK3A, RELA, HMGB1, FASN, ACAT1 , and MPI . Molecular docking showed that the binding energies of Tanshinone IIA with all targets were lower than -6.8 kcal/mol, with the strongest binding observed for SCN9A (-10.6 kcal/mol) and PIM1 (-10.2 kcal/mol). GO analysis revealed that the targets were significantly enriched in biological processes such as inflammatory response and interleukin regulation. KEGG analysis indicated that the main pathways involved were fatty acid metabolism, the AGE-RAGE signaling pathway, and the acute myeloid leukemia pathway. Conclusion: Tanshinone IIA may exert multi-dimensional protective effects in the treatment of myocardial infarction by acting on multiple targets such as SCN9A and PIM1, and by synergistically regulating key pathways including inflammatory response and fatty acid metabolism. This study provides a theoretical basis for elucidating its systematic mechanism of action and future clinical translation.