Network pharmacology analysis and clinical verification of Shenmai Injection in suppressing leukopenia after chemotherapy
OBJECTIVE To explore the mechanism of Shenmai Injection suppressing leukopenia after chemotherapy through network pharmacology and molecular docking technology and conduct clinical validations.METHODS The chemical components of Shenmai Injection were screened by the databases of TCMSP and BATMAN-TCM.And the database of Swis-starget was utilized for screening for the action targets of active components.Disease databases were utilized for screening the rel-evant disease targets for leukopenia.After taking intersection targets,"drug-component-target"network was established for GO function and KEGG pathway enrichment analysis.Protein interaction network was constructed and key targets were selected for molecular docking.From June 2021 to June 2023,60 patients on FOLFOX chemotherapy were selected and randomized into two groups of control and trial(n=30 each).In trial group,Shenmai Injection was dosed with chemotherapy.The levels of leukocyte,neutrophil,tumor necrosis factor,interleukin 6 and symptomatic treatment rate of human granulocyte stimulating factor injection were compared between two groups.RESULTS There were 59 active components,674 drug targets,1 394 disease targets for leukopenia and 147 intersection targets in Shenmai Injection.It involved 776 GO functions and 158 KEGG pathways of cancer and AGE-RAGE/PI3K-Akt signaling.PPI network visualization analysis revealed core target proteins such as AKT1,TNF,IL-6 and molecular docking of core targets with four active ingredients of reverse screening was performed.As compared with control group,absolute values of leukocytes and neutrophils after chemotherapy spiked and the levels of TNF-α and IL-6 level in trial group(P<0.05).There was a low usage rate of human granulocyte stimulating factor injection.CONCLUSION Shenmai Injec-tion may suppress leukopenia after chemotherapy through a multi-component,multi-target,multi-pathway mechanism.And serum levels of TNF-α and IL-6 are down-regulated.