文章基本信息

标题：Exploration of underlying molecular mechanism of Lycii Cortex in Treating Type 2 Diabetes Mellitus Based on Network Pharmacology and Molecular Docking
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作者：Dongjun Li ; Denghui Wang ; Shikai Yan 等
期刊名称：E3S Web of Conferences
印刷版ISSN：2267-1242
电子版ISSN：2267-1242
出版年度：2021
卷号：233
页码：2007
DOI：10.1051/e3sconf/202123302007
出版社：EDP Sciences
摘要：Objective: To explore the potential molecular mechanism of Lycii Cortex in treating type 2 diabetes mellitus (T2DM) by virtue of network pharmacology and molecular docking method. Methods : Ingredients of Lycii Cortex were collected from TCMSP and BATMAN-TCM databases, and the corresponding targets and T2DM-related targets were obtained respectively from SwissTargetPrediction and GenCards databases. Venn diagram was applied to derive the potential active components and effect targets of Lycii Cortex in the treatment of T2DM. GO enrichment analysis and KEGG pathway analysis were performed in the database of DAVID. Cytoscape 3.6.1 was used to produce the “core components-core targets” network. The molecular docking between core components and core targets was implemented through Autodock Vina. Results: Six core components and twelve core targets of Lycii Cortex in treating T2DM were identified. GO enrichment analysis and KEGG pathway analysis suggested the following signaling pathways and biological processes were involved in the treatment of T2DM by Lycii Cortex : PI3K-Akt signaling pathway, TNF signaling pathway, HIF-1 signaling pathway, Toll-like receptor signaling pathway, NOD-like receptor signaling pathway, and peptidyl-threonine phosphorylation, the positive regulation of cyclase activity, the positive regulation of genetic expression, and lipoprotein translocation. The binding results demonstrated a relatively high affinity between core components of Lycii Cortex , including kulactone, hederagenin, scopolin, etc., and core targets, containing IL6, PPARγ, TNF, and mTOR, indicating the efficacy of Lycii Cortex in treating T2DM. Conclusion: Lycii Cortex plays a role in the treatment of T2DM with its ingredients such as kulactone, linarin, hederagenin, and scopolin regulating glycometabolism, affecting cell apoptosis and weakening inflammatory response through targets like IL6, PPARγ, TNF, and mTOR.
其他摘要：Objective: To explore the potential molecular mechanism of Lycii Cortex in treating type 2 diabetes mellitus (T2DM) by virtue of network pharmacology and molecular docking method. Methods : Ingredients of Lycii Cortex were collected from TCMSP and BATMAN-TCM databases, and the corresponding targets and T2DM-related targets were obtained respectively from SwissTargetPrediction and GenCards databases. Venn diagram was applied to derive the potential active components and effect targets of Lycii Cortex in the treatment of T2DM. GO enrichment analysis and KEGG pathway analysis were performed in the database of DAVID. Cytoscape 3.6.1 was used to produce the “core components-core targets” network. The molecular docking between core components and core targets was implemented through Autodock Vina. Results: Six core components and twelve core targets of Lycii Cortex in treating T2DM were identified. GO enrichment analysis and KEGG pathway analysis suggested the following signaling pathways and biological processes were involved in the treatment of T2DM by Lycii Cortex : PI3K-Akt signaling pathway, TNF signaling pathway, HIF-1 signaling pathway, Toll-like receptor signaling pathway, NOD-like receptor signaling pathway, and peptidyl-threonine phosphorylation, the positive regulation of cyclase activity, the positive regulation of genetic expression, and lipoprotein translocation. The binding results demonstrated a relatively high affinity between core components of Lycii Cortex , including kulactone, hederagenin, scopolin, etc., and core targets, containing IL6, PPARγ, TNF, and mTOR, indicating the efficacy of Lycii Cortex in treating T2DM. Conclusion: Lycii Cortex plays a role in the treatment of T2DM with its ingredients such as kulactone, linarin, hederagenin, and scopolin regulating glycometabolism, affecting cell apoptosis and weakening inflammatory response through targets like IL6, PPARγ, TNF, and mTOR.