To study the therapeutic targets and related signal pathways of Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata in the treatment of chronic heart failure by network pharmacology and molecular docking for a better understanding of its potential mechanism.Methods:Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP) and UniProt were used to obtain the components and targets of Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata.The targets of chronic heart failure were downloaded from GeneCards and Online Mendelian Inheritance in Man(OMIM).The common targets of Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata and chronic heart failure were then identified.The protein-protein interactions(PPIs) were obtained by String,and the network was visualized in Cytoscape 3.8.0 to calculate the Degree value of each target.The top five Degree values were selected for molecular docking.Furthermore,the Gene ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed by David.Finally,all the information was input into Cytoscape 3.8.0 to construct the “Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata-components-targets-pathways-disease” network.Results:A total of 41 components from Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata and 13 051 chronic heart failure targets were obtained.The top five targets were AKT1,MAPK1,JUN,TP53 and TNF in terms of Degree.Based on the above data,we constructed a PPI network,which was mainly related to transcription regulation,signal transduction,apoptosis regulation,cell proliferation and other biological processes.KEGG analysis indicated target enrichments in HIF-1,MAPK,PI3K-AKT,and other heart failure-related signal pathways.Conclusion:Radix Astragali seu Hedysari-Radix Aconiti Lateralis Preparata could play a positive role in the treatment of chronic heart failure through multiple targets,such as AKT1,MAPK1,and JUN and multiple signal pathways,such as HIF-1 and MAPK signal pathways.The potential mechanism discussed in this study could provide reference for further experimental research.