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Chinese Traditional and Herbal Drugs ; (24): 3523-3530, 2018.
Article in Chinese | WPRIM | ID: wpr-851791

ABSTRACT

Objective: To explore the anti-inflammatory mechanism of Scutellarlae Radix (SR) by the network pharmacology. Methods: Firstly, the components in SR were searched through TCMSP database and screened with “Lipinski rule” and “Oral Bioavailability > 30%” rules. The targets of above components selected by PharmMapper web server and Cytoscape 3.4.0 was used to build a network between components and targets (component-target network, CTN). Secondly, “anti-inflammatory” targets was searched from Therapeutic Target Database (TTD) with keyword “anti-inflammatory”, and targets retrieved were used to build a protein-protein interaction (PPI) network based on the analysis by String database. To obtain anti-inflammatory targets of the active components in SR, the PPI network was fused with the CTN. Finally, the DAVID database was used to perform KEGG pathway enrichment analysis in order to explore the anti-inflammatory mechanism of SR. Results: Twenty-eight components in SR were obtained, including flavonoids such as baicalin, baicalein, wogonin, wogonoside, etc, alkaloids such as berberine, and epiberberine, and phenols such as dihydromyricetin, etc. Mitogen-activated protein kinase (MAPK14), tumor necrosis factor receptor superfamily 1A (TNFRSF1A), epidermal growth factor receptor (EGFR), and E-selectin (SELE) were the main targets of SR' anti-inflammatory effect. Salvigenin, epicatechin, and astragalusine mainly acted on MAPK14; Carthamidin acted on TNFRSF1A; Dihydromubutin A, 5,7,4’-trihydroxy-8-methoxyflavone, 5,7,4’-trihydroxy-8-methoxyflavanone, baicalin, and other components mainly acted on EGFR. There were 11 KEGG pathways, mainly related to TNF signaling pathways, MAPK signaling pathway, etc. Conclusion: There are three main anti-inflammatory mechanisms in SR, which can inhibit the production of inflammatory factors, inhibit the binding of inflammatory factors to their respective receptors, and block the initiation of inflammatory reactions.

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