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<p>To elucidate resveratrol’s (RES) effects on blood lipids and underlying mechanisms, this study integrated meta-analysis with network pharmacology and molecular dynamics simulations. Randomized controlled trials (RCTs) were systematically retrieved, screened, and assessed for quality, followed by meta-analysis. Separately, shared targets of RES and hyperlipidemia were identified, and protein–protein interaction networks were constructed using Cytoscape. Core targets were validated via molecular docking and 100&#xa0;ns molecular dynamics simulations. Meta-analysis of seven RCTs (<i>n</i> = 337) revealed that RES significantly reduced triglycerides (TG) but showed no significant effects on total cholesterol, low-density lipoprotein, or high-density lipoprotein. Network pharmacology identified 794 RES-hyperlipidemia overlapping targets, with PPI analysis prioritizing three pro-inflammatory hubs: Interleukin-6 (IL6), Interleukin-1β (IL1B), and tumor necrosis factor. Molecular dynamics simulations confirmed stable RES binding to these targets, with strong binding free energies of − 13.95, − 11.86, and − 11.28&#xa0;kcal/mol, respectively. RES specifically lowered TG but not other lipids, potentially through direct modulation of inflammatory pathways rather than classic lipid metabolism regulators. Comprehensive analysis indicated RES as a promising therapeutic candidate for hypertriglyceridemia.</p>

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Anti-inflammatory mechanism of resveratrol’s Triglyceride-lowering effect in hyperlipidemia: a meta-analysis integrated network pharmacology and molecular dynamics simulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月24日

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  • Yinyan Shao,
  • Junwei Shi

摘要

To elucidate resveratrol’s (RES) effects on blood lipids and underlying mechanisms, this study integrated meta-analysis with network pharmacology and molecular dynamics simulations. Randomized controlled trials (RCTs) were systematically retrieved, screened, and assessed for quality, followed by meta-analysis. Separately, shared targets of RES and hyperlipidemia were identified, and protein–protein interaction networks were constructed using Cytoscape. Core targets were validated via molecular docking and 100 ns molecular dynamics simulations. Meta-analysis of seven RCTs (n = 337) revealed that RES significantly reduced triglycerides (TG) but showed no significant effects on total cholesterol, low-density lipoprotein, or high-density lipoprotein. Network pharmacology identified 794 RES-hyperlipidemia overlapping targets, with PPI analysis prioritizing three pro-inflammatory hubs: Interleukin-6 (IL6), Interleukin-1β (IL1B), and tumor necrosis factor. Molecular dynamics simulations confirmed stable RES binding to these targets, with strong binding free energies of − 13.95, − 11.86, and − 11.28 kcal/mol, respectively. RES specifically lowered TG but not other lipids, potentially through direct modulation of inflammatory pathways rather than classic lipid metabolism regulators. Comprehensive analysis indicated RES as a promising therapeutic candidate for hypertriglyceridemia.