Network Pharmacology and Molecular Docking-Based Prediction of the Molecular Targets and Signaling Pathways of Ginseng in the Treatment of Parkinson's Disease

Abstract

Objective: The present study was aimed at exploring the molecular mechanism underlying the action of ginseng in the treatment of Parkinson's disease (PD) using network pharmacology. Methods: The main effective ginseng ingredients were obtained from the traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP) database and screened for oral bioavailability (OB), as well as drug-like properties (DL). A platform of PD targets was established using GeneCards and Online Mendelian Inheritance in Man (OMIM) databases, and then an “effective ingredient-target-disease” interaction network was constructed using Cytoscape 3.7.1 software. A STRING database was used to construct a protein–protein interaction (PPI) network, and the related protein interactions were analyzed. Finally, we performed functional analyses of core targets using the Gene Ontology (GO) and Kyoto Gene and Gene Encyclopedia (KEGG) pathway enrichment, and then conducted molecular docking of the effective ingredients with disease targets. Results: Ninety-seven effective ginseng ingredients and 168 potential targets of PD were identified in the present study. Network analysis showed that the targets were mainly involved in regulating cell metabolism, apoptosis, and other biological processes (BPs). Further, it was noted that the effects of the targets on treatment of PD involved regulation of several signaling pathways, such as mitogen-activated protein kinase (MAPK), advanced glycation end products (AGE), and receptors of advanced glycation end products (RAGE). The results of molecular docking showed that the active ginseng ingredients bind well with the targets of MAPK3 and MAPK14. Conclusion: The main active compounds of ginseng in the treatment of PD may be ginsenosides, and the molecular mechanism may be related to key targets such as MAPK3, MAPK14, and EGFR. The MAPK and AGE-RAGE signaling pathways may also be involved.