Abstract：Objective：To analyze the potential effective components of Sanqi Oral Liquid for arteriovenous fistula maturation failure and its mechanism through network pharmacology and molecular docking. Methods： A total of 25 active components were screened from Sanqi Oral Liquid by network pharmacology analysis. The data sets of GSE119296， GSE233264 and GSE220796 in GEO database were used to screen out the differential genes of arteriovenous fistula maturation failure. Disease targets were obtained from databases of GeneCards， OMIM and PharmGKB. Machine learning was used to screen out core disease targets. Cytoscape 3.8.0 software was used to construct a “drug active components-targets” network. Gene Ontology （GO） function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes（KEGG）pathway enrichment analysis of key targets were performed using the ggplot2 package and clusterProfiler of R3.6.4 software. Molecular docking verification was performed on the active components and predicted disease targets. Results：A total of 25 potential active components and two key targets from Sanqi Oral Liquid for arteriovenous fistula maturation failure were screened out. Among them， there were five core active components， namely quercetin， isorhamnetin， β - sitosterol， formononetin and kaempferol， and two core targets，namely KDR and MMP2. The results of GO function enrichment analysis covered wound healing，regulation of inflammatory response，response to xenobiotic stimulus，response to oxidative stress，etc. KEGG analysis was mainly enriched in fluid shear stress and atherosclerosis， AGE-RAGE signaling pathway in diabetic complications， HIF-1 signaling pathway， IL-17 signaling pathway， etc. Molecular docking results showed that quercetin， isorhamnetin， β-sitosterol， formononetin and kaempferol had high affinity with KDR and MMP2. Conclusion： Sanqi Oral Liquid may mediate fluid shear stress and atherosclerosis，AGE-RAGE，PI3K-AKT and other signaling pathways through the binding of quercetin and isorhamnetin with the main core targets of KDR and MMP2， and further intervene in arteriovenous fistula maturation failure.