Abstract： Objective： To analyze the medication patterns and mechanism of traditional Chinese medicine （TCM）in treating invasive pulmonary fungal disease（IPFD）. Methods：Clinical literature on TCM treatment of IPFD was collected from databases including CNKI. Medication patterns were analyzed， and the herb pair with the highest confidence was selected as the core combination for mechanism investigation. TCM components and targets were screened through TCMSP and Swiss Target Prediction databases， screening disease target genes from GeneCards to obtain herb disease intersection targets. A "herb-active component-intersection target" network was constructed. Protein-protein interaction（PPI）networks were obtained from STRING，followed by GO functional and KEGG pathway enrichmentanalysisusingMetascape.Moleculardockingvalidationwasperformed.Results：A totalof46articles involving 51 Chinese herbal medicine prescriptions and 111 herbs were included. Herbs exhibited balanced cold-warm properties， predominantly bitter，sweet，and acrid flavors，mainly acting on lung，spleen，and stomach meridians. Association rule and cluster analysis identified 12 herb pairs and 3 core combinations， with "Glycyrrhizae Radix et Rhizoma- Armeniacae Semen Amarum" showing the highest confidence. Investigation of this core pair revealed 144 herb-disease intersectiontargets，1593GOterms，and165KEGGpathways.Keyactivecomponentsincludedquercetin，isorhamnetin， and isoliquiritigenin，acting on targets like AKT1，EGFR，and SRC through cancer pathways and PI3K-AKT signaling pathway. Molecular docking confirmed stable binding between active components and targets. Conclusion：This study found that TCM treatment of IPFD combines clearing and tonifying strategies，with emphasis varying by syndrome type. Furthermechanisticexplorationofthecoreherbpairsuggests"GlycyrrhizaeRadixetRhizoma-ArmeniacaeSemen Amarum" may treat IPFD through active components like quercetin，isorhamnetin，isoliquiritigenin，and α-trihydroxy coprostanic acid modulating cancer pathways and PI3K-AKT signaling pathways，targeting AKT1，EGFR，SRC，and STAT3.