Mechanism of therapeutic action of Folium Artemisiae Argyi on Neuropathic pain based on network pharmacology and molecular docking technology

Abstract Objective To elucidate the mechanism of therapeutic action of Folium Artemisiae Argyi (FAA) on Neuropathic Pain (NP) based on network pharmacology, molecular docking and experimental verification. Methods The components of the FAA were screened from Traditional Chinese Medicine Systems Pharmacology database (TCMSP) and predicted their targets of action in the Swiss Target Predication platform. Then, retrieving the NP targets from Genecards and other disease databases. Thereby, the common targets of the medicine and the disease were screened out by Cytoscape 3.8.2 software, and the STRING database was used for Protein–Protein Interaction (PPI) network analysis, followed by Gene Ontology (GO) term enrichment by DAVID database, and pathway analysis was done using Kyoto Encyclopedia of Genes and Genomes (KEGG) to identify core targets, further we performed the molecular docking to obtain the binding efficiency between the components and the targets of proteins. After that, NP modeling of BV 2 cells induced by ATP was established to detect the protective effect of the four key components. The effectiveness of the results was further verified by in vitro experiments. Results The result showed that Chlorogenic Acid (CGA), Eupatilin (EUP), Ethyl Oleate (EO) and Ethyl Linoleate (ELO) are the key components dedicated to its neuroprotective effect. The neuroprotective mechanism may be related to AKT1, PIK3CA, JAK1, P2X4, P2X7 and other targets enriched in PI3K-Akt pathway. CGA, EUP, EO and ELO were able to protect against neurological damage caused by ATP, downgraded the activated P2X receptors and the above approach may be its protection mechanism. Conclusion The potential targets and biological effects of FAA in the treatment of NP were predicted in this study. The P2X receptor and PI3K-AKT signaling pathway may be key targets of FAA on ATP-induced NP cells.