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<p>To analyze the potential therapeutic value and mechanism of luteolin in age-related macular degeneration (AMD) using network pharmacology and cellular experiments. SHD-compound targets were retrieved from the TCMSP database, while AMD-related targets were extracted from OMIM and DisGeNET databases. Overlapping targets were identified via Venny 2.1. A PPI network was constructed using the STRING database, followed by functional enrichment analysis of overlapping targets via Metascape. Pharmacological networks were mapped using Cytoscape. For cellular experiments, the optimal concentration of luteolin was determined by CCK-8 assay. Human umbilical vein endothelial cells (HUVECs) were divided into: Control group (Without any intervention), Model group (VEGF165-induced model), and Treatment group (VEGF165-induced + luteolin). Angiogenesis was evaluated via scratch, transwell migration, invasion, and tube formation assays. VEGFA protein expression was assessed by Western blot. We identified 157 SHD-compound targets and 87 AMD-related targets, yielding 6 overlapping targets (ESR1, PON1, SOD1, APOB, VEGFA, IL6). PPI networks and enrichment analysis revealed that luteolin in SHD may inhibit AMD neovascularization via VEGFA signaling pathways. The concentration of luteolin (25 µmol/L) used in the experiments was selected based on the dose-response results. In vitro assays showed the Treatment group exhibited: significantly reduced horizontal migration (scratch assay, <i>p</i> &lt; 0.05), decreased vertical migration (transwell assay, <i>p</i> &lt; 0.05), suppressed invasion (<i>p</i> &lt; 0.05), and inhibited tube formation (<i>p</i> &lt; 0.05). Western blot confirmed reduced VEGFA expression in the treatment group (<i>p</i> &lt; 0.05). Luteolin alleviates angiogenesis in HUVECs by inhibiting VEGFA expression, highlighting its potential as a therapeutic candidate for neovascular AMD.</p>

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Luteolin alleviates angiogenesis in HUVECs by inhibiting VEGFA expression: integrating network pharmacology and experimental validation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月28日

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  • Sichong Yang,
  • Dan Mu,
  • Xiaoting Li

摘要

To analyze the potential therapeutic value and mechanism of luteolin in age-related macular degeneration (AMD) using network pharmacology and cellular experiments. SHD-compound targets were retrieved from the TCMSP database, while AMD-related targets were extracted from OMIM and DisGeNET databases. Overlapping targets were identified via Venny 2.1. A PPI network was constructed using the STRING database, followed by functional enrichment analysis of overlapping targets via Metascape. Pharmacological networks were mapped using Cytoscape. For cellular experiments, the optimal concentration of luteolin was determined by CCK-8 assay. Human umbilical vein endothelial cells (HUVECs) were divided into: Control group (Without any intervention), Model group (VEGF165-induced model), and Treatment group (VEGF165-induced + luteolin). Angiogenesis was evaluated via scratch, transwell migration, invasion, and tube formation assays. VEGFA protein expression was assessed by Western blot. We identified 157 SHD-compound targets and 87 AMD-related targets, yielding 6 overlapping targets (ESR1, PON1, SOD1, APOB, VEGFA, IL6). PPI networks and enrichment analysis revealed that luteolin in SHD may inhibit AMD neovascularization via VEGFA signaling pathways. The concentration of luteolin (25 µmol/L) used in the experiments was selected based on the dose-response results. In vitro assays showed the Treatment group exhibited: significantly reduced horizontal migration (scratch assay, p < 0.05), decreased vertical migration (transwell assay, p < 0.05), suppressed invasion (p < 0.05), and inhibited tube formation (p < 0.05). Western blot confirmed reduced VEGFA expression in the treatment group (p < 0.05). Luteolin alleviates angiogenesis in HUVECs by inhibiting VEGFA expression, highlighting its potential as a therapeutic candidate for neovascular AMD.