Abstract Objective Network pharmacology was used to analyze the effective active components and mechanism of Gynostemma pentaphyllum in the treatment of osteoporosis. Methods The effective active components and targets of Gynostemma pentaphyllum through the Traditional Chinese Medicine Systems pharmacology Database and Analysis Platform (TCMSP). Targets related to osteoporosis were identified by GeneCards,Therapeutic Target Database (TTD),Online Mendelian Inheritance in Man (OMIM) and Pharmacogenomics Knowledgebase (PharmGKB) databases. The intersection of drug targets and disease targets was analyzed by protein-protein interaction network analysis,GO function enrichment analysis and KEGG pathway analysis. Results Twenty-four effective active components of Gynostemma pentaphyllum, including quercetin, rhamnazin and isofucosterol, were obtained, corresponding to 217 targets. Through the GeneCards, TTD, OMIM and PharmGKB database, 4620 osteoporosis related targets and 121 intersection targets were obtained.The protein-protein interaction network analysis showed that JUN proto-oncogene (JUN), tumor protein P53 (TP53), AKT serine/threonine kinase 1 (AKT1), mitogen-activated protein kinase 1 (MAPK1), RELA protooncogene (RELA), estrogen receptor 1 (ESR1), mitogen-activated protein kinase 14 (MAPK14), Fos proto-oncogene(FOS), Myc proto-oncogene (MYC), signal transducer and activator of transcription 1 (STAT1) may be the core targets of the herb in the treatment of the disease.GO functional enrichment analysis showed 1964, 43 and 160 entries in biological process, cell composition and molecular function, respectively. KEGG pathway enrichment analysis revealed 162 signaling pathways involving lipids, atherosclerosis, chemical carcinogene-receptor activation, etc. Conclusion This study initially revealed that Gynostemma pentaphyllum can treat osteoporosis through multiple components, multiple targets and multiple pathways, and its molecular mechanism may be related to JUN, TP53,AKT1, MAPK1, RELA, ESR1, MAPK14, FOS, MYC, STAT1 and other targets. These pathways involve lipids and atherosclerosis, chemical carcinogenic receptor activation, fluid shear stress and atherosclerosis, which lay a foundation for further research.
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