Objective: In this study, the effects and signaling pathways of Nelumbinis folium in the treatment of hyperlipidemia were analyzed based on network pharmacology and molecular docking. Materials and Methods: The main components and targets of Nelumbinis folium were searched through traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP), and the active components were selected according to their oral availability and drug-like properties. The main targets of hyperlipidemia were identified using the DisGeNET database. Venny 2.1.0 was used to take the intersection of both targets, which were submitted to the STRING database to construct the protein-protein interaction network model. The Database for Annotation, Visualization and Integrated Discovery 6.7 was used to conduct gene ontology and Kyoto Encyclopedia of Gene and Genome pathway enrichment analyses of the targets. Cytoscape 3.7.1 was used to construct the component-target-pathway network. AutoDock Vina molecular docking software was used to study the binding effect and mechanism of the core components and targets of N. folium. Results: Fifteen active components of N. folium and 195 potential targets were selected through TCMSP, whereas 4216 targets for hyperlipidemia were selected from DisGeNET. Further, 138 potential cross-targets of hyperlipidemia were identified. A network of component-target-pathway was constructed. Quercetin, kaempferol, and isorhamnetin were the core components, which played an important role in anti-hyperlipidemia, mainly through the non-alcoholic fatty liver disease and insulin resistance (IR) signaling pathways. Molecular docking results showed that quercetin had the lowest docking energies with peroxisome proliferator activated receptor α, peroxisome proliferator-activated receptor γ, INSR (-6.20,-10.00, and -8.40 (kcal/mol, respectively). The binding mode was mainly hydrogen bonds and van der Waals forces. Conclusions: The active components of N. folium may regulate lipid metabolism by participating in the signaling pathways of non-alcoholic fatty liver disease and IR.