Exploring the Effect of Ginsenosides on Thymocyte-Thymic Epithelial Intercellular Mitochondrial Transfer Based on Network Pharmacology
DOI:
https://doi.org/10.62767/jecacm604.0230Keywords:
mitochondria transfer, network pharmacology, ginsenosides, 20(s)-Protopanaxadiol, protopanaxatriolAbstract
Background: The function of immune cells in thymus microenvironment is closely related to mitochondria. Ginsenoside, as the main active metabolite of ginseng, has immunomodulatory effects, but its effect on mitochondrial transfer between thymocytes and thymic epithelial cells is not clear. To predict the effect of ginsenosides on mitochondrial transfer between thymocytes and thymic epithelial cells based on network pharmacology. Methods: With the database and analysis platform of systematic pharmacology of traditional Chinese medicine, PharmMapper and Swiss Target Prediction were used for ingredient screening and corresponding target prediction. The targets of mitochondria, thymocytes and thymic epithelial cells were obtained by using the Genome Annotation Database Platform (GeneCards) database. The Metascape database was applied for enrichment analysis of gene ontology (GO) and Kyoto encyclopedia of Genes and genomes (KEGG) to predict the mechanism of action. Results: KEGG pathway enrichment analysis showed that it was related to mitochondria-related pathway, including phosphatidylinositide 3-kinases/protein kinase B (PI3K-Akt) signaling pathway, cyclic adenosine monophosphate (cAMP) signaling pathway, cyclic guanosine monophosphate/protein kinase G (cGMP-PKG) signaling pathway, and Ras-related protein 1 (Rap1) signaling pathway. GO function positively regulated phosphorus metabolism, protein serine kinase activity, and cell response to estrogen. Conclusions: Ginsenogenin may promote mitochondrial transfer between thymocyte and thymic epithelial cells and improve mitochondrial dysfunction. 20(s)-Protopanaxadiol (PPD) promotes mitochondrial generation through cAMP signaling pathway, while Propanaxantriol (PPT) regulates mitochondria through cGMP-PKG signaling pathway and Rap1 signaling pathway. The above analysis results provide new clues and hypotheses for understanding the immunomodulatory effects of ginsenosides, but their exact effects and molecular mechanisms need to be confirmed by further experimental studies.
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The data presented in this study are available on request from the corresponding author.
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