Potential Mechanisms of Baicalin against Viral Pneumonia Revealed by Network Pharmacology and Molecular Docking

Abstract

While baicalin exhibits therapeutic potential against viral pneumonia, its systems-level mechanisms remain elusive. This study integrates network pharmacology, transcriptomic profiling, and molecular docking to decode these multi-target interactions. By mapping baicalin-associated genes against viral pneumonia profiles, we identified 223 shared targets. Subsequent network topology analysis prioritized core hub genes (e.g., AKT1, IL6, TP53, CTNNB1, and BCL2), whose clinical relevance was corroborated using a severe COVID-19 transcriptomic dataset (GSE171110). Specifically, the expression data revealed significant dysregulation in key inflammatory and apoptotic mediators, including the marked upregulation of MMP9, STAT3, and CASP3. Functional enrichment linked these networks primarily to PI3K-Akt signaling, MAPK cascades, and host antiviral immune responses. Furthermore, molecular docking confirmed high-affinity binding (–7.5 to –9.0 kcal/mol) between baicalin and the top five hub proteins. These findings delineate the specific kinase and cytokine networks mediating baicalin’s protective effects, providing an empirically supported framework for future experimental validation.