Exploring the therapeutic targets and mechanisms of Fructus Meliae Toosendan in acute myeloid leukemia based on network pharmacology
Objective To analyze the potential therapeutic targets and molecular mechanisms of Fructus Meliae Toosendan(FMT)in the treatment of acute myeloid leukemia(AML),based on network pharmacology and bioinformatic approaches.Methods The relevant targets of FMT and AML were identified through TCMSP,DrugBank,Uniprot,SwissTargetPrediction and other databases,respectively,and the potential targets of FMT acting on AML were obtained by Venn analysis,which was combined with KEGG and GO analyses to explore the mechanisms of FMT exerting its anti-AML effects.A protein-protein interaction network was constructed based on the STRING database,identifying core functional genes.Molecular docking techniques were employed to analyze the interactions between small molecule drugs and core targets related to the disease.Additionally,the GEPIA database was utilized to investigate proteins closely associated with patient prognosis.Results Network pharmacology analysis revealed that FMT may exert its anti-AML effects by targeting 185 proteins.GO analysis and KEGG pathway enrichment indicated that FMT influences biological processes such as apoptosis and regulates signaling pathways like PI3K-Akt and MAPK,affecting the occurrence and progression of AML.The active components of FMT exhibited binding activity with six core protein targets,suggesting that targeting these proteins could play a role in anti-AML effects.Additionally,analysis from the GEPIA database showed that the expression of the proto-oncogene tyrosine-protein kinase Src(SRC)is closely related to the prognosis of AML patients,with low SRC expression correlating with better outcomes,indicating that SRC may be a potential target for the anti-AML effects of FMT.Conclusion The bioactive constituents of FMT may exert anti-AML effects through the regulation of multiple target proteins,the induction of apoptosis,and the modulation of signaling pathways,including PI3K-Akt and MAPK pathways.SRC could potentially serve as one of the targets through which FMT improves AML prognosis.