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Background <p>Borneol essential oil was obtained by distillation with steam from the branches and leaves of <i>Cinnamomum camphora</i> chvar. <i>Borneol</i> alleviates learning and memory impairments, but it is not known whether and how it exerts an effect on Alzheimer’s Disease (AD). To explore the possible mechanisms of borneol essential oil in AD via network pharmacology and molecular docking.</p> Methods <p>Gas chromatography–time-of-flight mass spectrometry (GC-TOFMS) was used to characterize the volatile constituents of borneol essential oil, followed by network pharmacology analysis to elucidate the core targets and key signaling pathways underlying its potential therapeutic effects on Alzheimer’s disease. Molecular docking was used to find out the active components of the essential oil of borneol. Behavioral tests, enzyme-linked immunosorbent assay (ELISA), western blotting (WB), and immunohistochemistry (IHC) were run in an amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mouse AD model. The impact of borneol essential oil on improving AD symptoms and its mechanisms, mainly focusing on the anti-inflammatory ones, was explored.</p> Results <p>Five core targets of the essential oil—ESR1, MAPK3, PGR, ERBB2, and MAPK1—were treated with AD. The NF-κB pathway was the main signaling pathway and guaiol was the main active ingredient. And also borneol essential oil alleviated the cognitive deficit, motor deficit, and pathological phenomena in APP/PS1 model mice. Mechanically, they were correlated with downregulation of the extracellular signal-regulated kinase (ERK)/nuclear factor kappa B (NF-κB) signaling pathway, suggesting anti-inflammatory effects that may contribute to the modulation of AD-related pathology.</p> Conclusion <p>Borneol essential oil alleviated neuroinflammatory responses and ameliorated AD-like pathological features in APP/PS1 mice through modulation of the ERK/NF-κB pathway.</p>

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Exploration of borneol essential oil function in the treatment of Alzheimer’s disease based on network pharmacology and experimental validation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月4日

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  • Chunshan You,
  • Shijia Wu,
  • Yali Zhang,
  • Qingxian Li,
  • Yuying Cui,
  • Yani Wu

摘要

Background

Borneol essential oil was obtained by distillation with steam from the branches and leaves of Cinnamomum camphora chvar. Borneol alleviates learning and memory impairments, but it is not known whether and how it exerts an effect on Alzheimer’s Disease (AD). To explore the possible mechanisms of borneol essential oil in AD via network pharmacology and molecular docking.

Methods

Gas chromatography–time-of-flight mass spectrometry (GC-TOFMS) was used to characterize the volatile constituents of borneol essential oil, followed by network pharmacology analysis to elucidate the core targets and key signaling pathways underlying its potential therapeutic effects on Alzheimer’s disease. Molecular docking was used to find out the active components of the essential oil of borneol. Behavioral tests, enzyme-linked immunosorbent assay (ELISA), western blotting (WB), and immunohistochemistry (IHC) were run in an amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mouse AD model. The impact of borneol essential oil on improving AD symptoms and its mechanisms, mainly focusing on the anti-inflammatory ones, was explored.

Results

Five core targets of the essential oil—ESR1, MAPK3, PGR, ERBB2, and MAPK1—were treated with AD. The NF-κB pathway was the main signaling pathway and guaiol was the main active ingredient. And also borneol essential oil alleviated the cognitive deficit, motor deficit, and pathological phenomena in APP/PS1 model mice. Mechanically, they were correlated with downregulation of the extracellular signal-regulated kinase (ERK)/nuclear factor kappa B (NF-κB) signaling pathway, suggesting anti-inflammatory effects that may contribute to the modulation of AD-related pathology.

Conclusion

Borneol essential oil alleviated neuroinflammatory responses and ameliorated AD-like pathological features in APP/PS1 mice through modulation of the ERK/NF-κB pathway.