Abstract: The study aimed to explore the mechanism of Cistanches Herba in treatment of Parkinson’s disease based on network pharmacology and molecular docking. The active components in Cistanches Herba were selected as candidate compounds by the TCMSP. And the target information of Cistanches Herba was obtained by PubChem and sea database. The target information of Parkinson’s disease was obtained by GeneCard database and the common target gene information was obtained by comparing traditional Chinese medicine and disease targets. PPI network was constructed by means of STRING. The key target genes were enriched by GO and KEGG pathway in DAVID 6.8 database. The Cytoscape software was applied to construct the network diagram of traditional Chinese medicine-chemical compound-target. The gene targets in the network were sorted according to the degree value, the first five key targets were selected. Finally, the five key targets were in connection with the effective active components of Cistanches Herba by using AutoDock Vina tool. In the end, the results showed that 6 active components were screened from Cistanches Herba beta-sitosterol, arachidonate, suchilactone, Yangambin, quercetin, Marckine. 308 prediction targets were obtained by intersection, which were analyzed by PPI. 38 key target genes were filtered out, and the key target genes were enriched by GO and KEGG pathway. Finally, it was found that GO rich BP includes intracellular signal transduction; CC analysis mainly included protein complex, mitochondrion; MF results mainly included ATP binding, protein complex binding. KEGG pathway enrichment mainly included PI3K/Akt, miRNAs, HIF-1, TNF, FOXO signal pathways, etc. The first five key targets were MAPK8, ESR1, SRC, JAK2 and AKT1. The results of molecular docking showed that the six active components of Cistanches Herba had good binding activity with five key targets. This study found that Cistanches Herba could play a multi-component, multi-channel and multi-target synergistic role in the treatment of Parkinson's disease by protecting mitochondrial function, regulating protein activity, regulating autophagy and inhibiting neuroinflammatory response.