天然产物研究与开发 ›› 2026, Vol. 38 ›› Issue (4): 873-882.doi: 10.16333/j.1001-6880.2026.4.018 cstr: 32307.14.1001-6880.2026.4.018

• 数据研究 • 上一篇    下一篇

基于网络药理学和体外实验的川芎抗SH-SY5Y细胞氧化损伤研究

张  敏1，李  学2，袁志臻1，任传忠1*，李  玮2*   

  1. 1信阳职业技术学院医学院，信阳 464000；2河南省人民医院，郑州 450000
  • 出版日期:2026-04-27 发布日期:2026-04-24
  • 基金资助:
    河南省医学科技攻关计划（SBGJ202002005）；河南省卫健委医学教育研究项目（WJLX2023248）

Effect of Ligusticum chuanxiong against oxidative damage in SH-SY5Y cells based on network pharmacology and in vitro experiments

ZHANG Min1,LI Xue2,YUAN Zhi-zhen1,REN Chuan-zhong1*,LI Wei2*   

  1. 1School of Medicine,Xinyang Vocational Technical College,Xinyang 464000,China;2Henan Provincial People′s Hospital,Zhengzhou 450000,China
  • Online:2026-04-27 Published:2026-04-24

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摘要：

研究川芎治疗帕金森病（Parkinson's disease，PD）和阿尔茨海默病（Alzheimer's disease，AD）的关键活性成分及相关机制。首先，采用网络药理学方法筛选川芎治疗PD和AD的活性成分及作用靶点，并构建“药物-疾病-成分-靶点”多维互作网络。进一步构建1-甲基-4-苯基吡啶离子（1-methyl-4-phenylpyridinium，MPP+）及β-淀粉样蛋白（β-amyloid protein，Aβ）片段Aβ25-35诱导的人神经母细胞瘤细胞SH-SY5Y氧化损伤模型，通过检测细胞活力、氧化应激指标及关键信号通路的表达探索其作用机制。结果显示，杨梅酮（myricanone，MyR）为川芎关键活性成分，可能通过调控糖原合酶激酶-3β（glycogen synthase kinase-3 beta，GSK-3β）等核心靶点发挥神经保护作用。此外，MyR可显著减轻MPP+/Aβ25-35诱导的SH-SY5Y细胞氧化损伤，提升细胞活力，并促进磷脂酰肌醇-3-激酶（phosphatidylinositol-3-kinase，PI3K）、蛋白激酶B（protein kinase B，AKT）和GSK-3β的磷酸化，该作用可被通路抑制剂逆转。综上，MyR通过PI3K/AKT/GSK-3β信号轴增强细胞抗氧化能力，拮抗MPP+/Aβ25-35诱导的神经元氧化损伤，提示其在开发PD和AD治疗药物中具有潜在应用价值。

关键词: 杨梅酮, 川芎, 氧化损伤, 网络药理学, PI3K/AKT/GSK-3β信号通路

Abstract:

This study explored the key active components of Ligusticum chuanxiong and their mechanisms in treating Parkinson's disease (PD) and Alzheimer's disease (AD). Initially, network pharmacology was employed to screen active ingredients and therapeutic targets of L. chuanxiong for PD and AD, constructing a multi-dimensional interaction network of "drug-disease-component-target". Then, an oxidative damage model in human neuroblastoma SH-SY5Y cells was established using 1-methyl-4-phenylpyridinium (MPP⁺) and β-amyloid fragment Aβ25-35. Cellular viability, oxidative stress markers, and signaling pathway activation were evaluated to investigate the underlying mechanisms. Results revealed myricanone (MyR) as the pivotal active component, exerting neuroprotection by modulating core targets such as glycogen synthase kinase-3β (GSK-3β). MyR significantly alleviated MPP⁺/Aβ25-35-induced oxidative damage in SH-SY5Y cells, enhanced cell viability, and promoted phosphorylation of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT), and GSK-3β. These effects were reversed by pathway inhibitors. Collectively, MyR enhanced cellular antioxidant capacity via the PI3K/AKT/GSK-3β signaling axis and ameliorated MPP+/Aβ25-35-induced neuronal oxidative damage, highlighting its potential application for PD/AD drug development.

Key words:

myricanone, Ligusticum chuanxiong, oxidative damage, network pharmacology, PI3K/AKT/GSK-3β pathway

中图分类号:  R285.5

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