Objective To explore the mechanism of Huangqi（Radix Astragali）-Taizishen（Radix Pseudostellariae） drug pair on reducing the cardiotoxicity of anthracyclines based on network pharmacology. Methods The active ingredients and targets of the herbal pair Huangqi-Taizishen were screened from the TCMSP database

the chemistry database and the PharMapper database. Screen the disease targets of anthracycline cardiotoxicity through GeneCards database and OMIM database. Venny 2.1 online analysis tool was used to construct a Venn diagram to obtain the common target of drugs and disease. The STRING platform was used to construct the protein-protein interaction relationship of the common target. The GO function analysis and the KEGG pathway enrichment analysis of the common target were performed using the R software

and the results were visualized by Cytoscape 3.7.1 software. Results There were 21 main active ingredients of Huangqi-Taizishen on reducing cardiotoxicity of anthracyclines

and 39 common targets of drug targets and disease targets. Quercetin（degree=32）

luteolin（degree=17）

kaempferol（degree=12）

acacetin（degree=7） and β-sitosterol（degree=7） were the key active ingredients

and AKT1

MAPK1

MAPK8 and CASP3 were the key targets. GO analysis showed that biological processes were mainly enriched in responses to oxidative stress

reactive oxygen species

metal ions

and apoptosis signaling pathway etc.; molecular functions were mainly reflected in phosphatase binding

antioxidant capacity

protein phosphatase binding

etc.; cell components were involved with membrane rafts

membrane microstructure domains

membrane regions

etc. KEGG analysis showed that 115 signaling pathways were enriched

and the pathways related to cardiotoxicity of anthracyclines were PI3 K/AKT signaling pathway

MAPK signaling pathway

HIF-1 signaling pathway and apoptosis signaling pathway. Conclusion Huangqi-Taizishen drug pair can reduce the cardiotoxicity of anthracyclines（chemotherapeutics） through anti-oxidative stress

anti-apoptosis

and regulation of metal ion metabolism.