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<p>Myricanone (MYR) is the active component of <i>Chuanxiong Rhizoma</i>, which has the potential to reduce blood lipids and anti-atherosclerosis.&#xa0;To explore the potential mechanism of MYR in the treatment of ischemic cerebral infarction (ICI) injury.&#xa0;This study employed network pharmacology to screen the active components of <i>Chuanxiong Rhizoma</i> and identify its potential targets. Through protein-protein interaction (PPI) network analysis, MAPK14 was identified as a core hub gene. Subsequently, molecular docking validated the binding affinity between MYR and MAPK14. To assess MAPK14’s clinical relevance, RT-qPCR measured its expression levels in peripheral blood mononuclear cells (PBMCs) from ICI patients, correlating it with disease severity (NIHSS score) and prognostic indicators (mRS score). Furthermore, the neuroprotective effects of MYR and its regulatory mechanism on MAPK14 were validated through an oxygen-glucose deprivation (OGD) in vitro model using HMC3 microglia and behavioral tests (rotarod test and Morris water maze) in a mouse ICI model.&#xa0;Five effective components of <i>Chuanxiong Rhizoma</i> were identified. They targeted 44 genes, of which MAPK14 was the core target. Molecular docking experiments showed that MYR had a strong binding affinity with MAPK14. In addition, MAPK14 expression in the PBMCs of ICI patients was positively correlated with disease severity and poor prognosis. In vitro and in vivo experiments confirmed that MYR significantly alleviated OGD-induced human microglia damage and improved ICI mice’s motor, learning, and memory deficits by down-regulating the expression of MAPK14.&#xa0;MYR may effectively inhibit ICI development by down-regulating MAPK14, providing a scientific basis for clinical application in ICI.</p> Graphical Abstract <p></p>

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Network Pharmacology and Molecular Docking Reveal Myricanone’s Role in Alleviating Ischemic Cerebral Infarction via Targeting MAPK14

  • 期刊论文

  • 发表日期：

    2026年4月24日

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  • Bingbing Zhao,
  • Jie Zhang

摘要

Myricanone (MYR) is the active component of Chuanxiong Rhizoma, which has the potential to reduce blood lipids and anti-atherosclerosis. To explore the potential mechanism of MYR in the treatment of ischemic cerebral infarction (ICI) injury. This study employed network pharmacology to screen the active components of Chuanxiong Rhizoma and identify its potential targets. Through protein-protein interaction (PPI) network analysis, MAPK14 was identified as a core hub gene. Subsequently, molecular docking validated the binding affinity between MYR and MAPK14. To assess MAPK14’s clinical relevance, RT-qPCR measured its expression levels in peripheral blood mononuclear cells (PBMCs) from ICI patients, correlating it with disease severity (NIHSS score) and prognostic indicators (mRS score). Furthermore, the neuroprotective effects of MYR and its regulatory mechanism on MAPK14 were validated through an oxygen-glucose deprivation (OGD) in vitro model using HMC3 microglia and behavioral tests (rotarod test and Morris water maze) in a mouse ICI model. Five effective components of Chuanxiong Rhizoma were identified. They targeted 44 genes, of which MAPK14 was the core target. Molecular docking experiments showed that MYR had a strong binding affinity with MAPK14. In addition, MAPK14 expression in the PBMCs of ICI patients was positively correlated with disease severity and poor prognosis. In vitro and in vivo experiments confirmed that MYR significantly alleviated OGD-induced human microglia damage and improved ICI mice’s motor, learning, and memory deficits by down-regulating the expression of MAPK14. MYR may effectively inhibit ICI development by down-regulating MAPK14, providing a scientific basis for clinical application in ICI.

Graphical Abstract