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<p>Ershiwei Chenxiang Pill (ECP) is effective in treating cardiovascular diseases including hypertension. High-altitude hypertension (HAH) is pathophysiologically distinct from general hypertension, primarily due to chronic hypoxia-induced mechanisms such as aberrant activation of the hypoxia-inducible factor (HIF) pathway and altered vascular remodeling. The molecular mechanism of ECP against HAH remains unclear. This study aims to elucidate this mechanism using network pharmacology and molecular docking.&#xa0;The effective components and target proteins of ECP were screened by the TCMSP database and TCMID database. The HAH genes were retrieved from NCBI, OMIM, and GeneCards databases. Protein-protein interaction (PPI) network was constructed to screen core targets. The distribution of the target in the organ was also assessed. The GO and KEGG enrichment analysis was carried out by the DAVID6.8 database. Finally, AutoDock 4.2.6 software was used for molecular docking verification.&#xa0;A total of 125 active components and 308 potential targets from ECP were identified, with 57 overlapping targets with HAH. PPI analysis revealed 14 key targets. GO analysis yielded 397 biological processes, 39 cellular components, and 52 molecular functions. KEGG analysis identified 207 pathways, among which the HIF-1 signaling pathway, Fluid shear stress and atherosclerosis were highlighted as most biologically relevant to HAH. Molecular docking confirmed strong binding affinities between four key components (apigenin, (-)-epigallocatechin-3-gallate, chrysoeriol, baicalein) and six core targets (VEGFA, PPARG, HIF1A, ESR1, MMP9, CAV1), with binding energies ranging from − 6.7 to -9.2&#xa0;kcal/mol.&#xa0;This study systematically reveals that ECP may treat HAH through multi-component, multi-target, and multi-pathway mechanisms, with a core emphasis on modulating hypoxia-responsive pathways (e.g., HIF-1) and vascular function. These findings offer novel insights into the mechanistic basis of ECP in HAH treatment and provide a foundation for further experimental validation.</p>

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Study on the mechanism of Ershiwei Chenxiang Pills in the treatment of high altitude hypertension based on network pharmacology and molecular docking analysis

  • 期刊论文

  • 发表日期：

    2026年1月27日

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  • Dianzhen Li,
  • Mengnan Hou,
  • Shan Wang,
  • Wenjing Wang,
  • Yan Yan,
  • Qingyun Yang,
  • Shuli Du,
  • Tainbo Jin,
  • Tianbo Jin

摘要

Ershiwei Chenxiang Pill (ECP) is effective in treating cardiovascular diseases including hypertension. High-altitude hypertension (HAH) is pathophysiologically distinct from general hypertension, primarily due to chronic hypoxia-induced mechanisms such as aberrant activation of the hypoxia-inducible factor (HIF) pathway and altered vascular remodeling. The molecular mechanism of ECP against HAH remains unclear. This study aims to elucidate this mechanism using network pharmacology and molecular docking. The effective components and target proteins of ECP were screened by the TCMSP database and TCMID database. The HAH genes were retrieved from NCBI, OMIM, and GeneCards databases. Protein-protein interaction (PPI) network was constructed to screen core targets. The distribution of the target in the organ was also assessed. The GO and KEGG enrichment analysis was carried out by the DAVID6.8 database. Finally, AutoDock 4.2.6 software was used for molecular docking verification. A total of 125 active components and 308 potential targets from ECP were identified, with 57 overlapping targets with HAH. PPI analysis revealed 14 key targets. GO analysis yielded 397 biological processes, 39 cellular components, and 52 molecular functions. KEGG analysis identified 207 pathways, among which the HIF-1 signaling pathway, Fluid shear stress and atherosclerosis were highlighted as most biologically relevant to HAH. Molecular docking confirmed strong binding affinities between four key components (apigenin, (-)-epigallocatechin-3-gallate, chrysoeriol, baicalein) and six core targets (VEGFA, PPARG, HIF1A, ESR1, MMP9, CAV1), with binding energies ranging from − 6.7 to -9.2 kcal/mol. This study systematically reveals that ECP may treat HAH through multi-component, multi-target, and multi-pathway mechanisms, with a core emphasis on modulating hypoxia-responsive pathways (e.g., HIF-1) and vascular function. These findings offer novel insights into the mechanistic basis of ECP in HAH treatment and provide a foundation for further experimental validation.