%0 Journal Article
%T Mechanism of mangiferin in the treatment of oral submucous fibrosis based on Gene Expression Omnibus database chip mining combined with network pharmacology and molecular docking.
%A Song Z
%A Yang C
%A Zhang Y
%A Zhang Z
%A Ren T
%A Zhang X
%A Li X
%J Hua Xi Kou Qiang Yi Xue Za Zhi
%V 42
%N 4
%D 2024 Aug 1
%M 39049631
暂无%R 10.7518/hxkq.2024.2024050
%X <B>OBJECTIVE: </B>This study aims to investigate the primary target and potential mechanism of mangiferin (MF) in treating oral submucous fibrosis (OSF) through Gene Expression Omnibus (GEO) database chip mining, network pharmacology, and molecular docking techniques.<BR><B>METHODS: </B>Potential therapeutic targets for OSF were identified using GEO chip data. The potential targets of MF were predicted, and disease-related targets for OSF were collected from databases. A Venn diagram was created using the EVenn platform to identify overlapping targets. The protein-protein interaction (PPI) network was constructed using the STRING database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using the DAVID platform. Cytoscape 3.10.1 software was used to visualize a drug-target-pathway-disease network, while AutoDocktools 1.5.6 software was employed for molecular docking analysis.<BR><B>RESULTS: </B>A total of 356 potential targets for MF and 360 disease-related targets for OSF were obtained from multiple databases. The top 15 key target proteins in the PPI network were selected as significant candidates. GO function and KEGG pathway enrichment analyses revealed that MF treatment primarily involved advanced glycation end products-receptor (AGE-RAGE), epidermal growth factor receptor (EGFR), and other signaling pathways associated with OSF pathogenesis. Molecular docking analysis demonstrated that MF exhibited a strong binding activity toward AKT serine kinase 1 (AKT1), tumor necrosis factor (TNF), and other core targets.<BR><B>CONCLUSIONS: </B>These findings suggest that MF may exert its therapeutic effects on OSF through a multitarget approach involving various signaling pathways.<BR>目的: 基于基因表达综合（GEO）数据库芯片挖掘、网络药理学及分子对接技术探讨芒果苷（MF）治疗口腔黏膜下纤维化（OSF）的核心作用靶标及潜在作用机制。方法: 基于GEO芯片挖掘OSF的潜在治疗靶点，利用数据库预测MF潜在作用靶标和收集OSF疾病靶标，使用EVenn平台绘制维恩图，STRING数据库绘制蛋白质互作（PPI）网络，DAVID平台进行基因本体论（GO）和京都基因与基因组百科全书（KEGG）富集分析，Cytoscape 3.10.1软件绘制药物—靶标—通路—疾病网络图，AutoDocktools 1.5.6软件进行分子对接分析及可视化。结果: 从多种数据库挖掘得到MF潜在靶标356个，OSF疾病靶标360个，选取PPI网络中排名前15个关键靶蛋白，GO功能及KEGG通路富集分析结果显示，MF治疗OSF主要涉及高级糖基化终末产物-受体（AGE-RAGE）、表皮生长因子受体（EGFR）等信号通路。分子对接显示，MF与丝氨酸蛋白激酶（AKT1）、肿瘤坏死因子（TNF）等核心靶点有较佳结合活性。结论: MF可能通过多靶点、多途径的方式对OSF发挥治疗作用。.