Mechanism and Molecular Targets of Songhe Guxue Formula for Treating Cancer Therapy-Introduced Thrombocytopenia—Based on Clinical Observation, Network Pharmacology, and Molecular Docking

Background Cancer therapy-induced thrombocytopenia (CTIT) is a common complication that compromises the efficacy and safety of anticancer treatments, with current therapeutic options remaining limited. Songhe Guxue Formula (SHGXF) is an empirical formulation developed based on the Traditional Chinese Medicine (TCM) principle of “supplementing qi and nourishing blood, strengthening the spleen and kidney.” Preliminary clinical observations have suggested its potential in managing CTIT; however, its underlying mechanisms remain unclear. This study aims to systematically predict the pharmacodynamic material basis, core targets, and signaling pathways of SHGXF against CTIT using network pharmacology for the first time, thereby providing a scientific foundation for its clinical application. Methods Active ingredients of SHGXF and their corresponding targets were retrieved from the TCMSP and HERB databases. Disease targets related to CTIT were collected from GeneCards and OMIM. Common targets were identified by intersecting the drug and disease targets. The “drug–ingredient–target” network and protein–protein interaction (PPI) network were constructed using Cytoscape software to screen core targets. Finally, Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed to elucidate the potential biological processes and signaling pathways involved. To evaluate the interactions between bioactive ingredients and central target proteins, molecular docking simulations were conducted. Results A total of 40 active ingredients and 566 corresponding targets of SHGXF were screened, along with 1036 CTIT-related targets. Among them, 104 common targets were identified. Network analysis revealed key active ingredients such as quercetin and core targets including AKT1,MTOR, PIK3CA, and GSK3B. Enrichment analysis showed that these targets were significantly associated with biological processes such as “cellular response to chemical stress” and “myocyte proliferation,” and were mainly involved in pathways including the PI3K–Akt signaling pathway, proteoglycans in cancer, and JAK–STAT signaling pathway. Conclusion This study suggests that SHGXF alleviates CTIT through a multi-component, multi-target, multi-pathway mechanism, involving quercetin, core targets like TP53 and AKT1, and the PI3K-Akt pathway, thereby reducing oxidative stress and promoting megakaryocyte differentiation.