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Peer-reviewedCC BY-NCPulmonary circulation

Integrated Network Pharmacology and Experimental Validation Implicate AKT1‐Associated Signaling in the Protective Effects of Panax notoginseng Against Pulmonary Arterial Hypertension

  • YiFan Sheng1
  • ZhiMeng Lu2
  • TianYu Wang3
  • HuiLin Tang4
  • XinYao Liu1
  • ZhiHao Zhao5
  • Praise Audax Rukonge5
  • GuiPing Yu1,2
5 affiliations
  1. 1Department of Central Laboratory Wuxi Key Laboratory of Biomaterials for Clinical Application, Jiangyin Clinical College of Xuzhou Medical University Wuxi P. R. China.
  2. 2Shanghai Public Health Clinical Center (Fudan University) Jinshan Shanghai China.
  3. 3Department of Thoracic and Cardiovascular Surgery The Affiliated Jiangyin Hospital of Nantong University Wuxi Jiangsu China.
  4. 4Department of Cardiology The Second Affiliated Hospital of Soochow University Suzhou China.
  5. 5Department of Cardiothoracic Surgery The Affiliated Hospital of Xuzhou Medical University Xuzhou Jiangsu China.
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Abstract

Pulmonary arterial hypertension (PAH) is a progressive and fatal cardiopulmonary disease characterized by pulmonary vascular remodeling, endothelial dysfunction, inflammation, and increased pulmonary vascular resistance. Despite advances in targeted therapies, effective treatment options remain limited. This study investigated the molecular mechanisms underlying the therapeutic effects of Panax notoginseng against PAH through integrated computational and experimental validation. Network pharmacology was employed to identify the bioactive compounds and therapeutic targets of Panax notoginseng. Functional enrichment, protein-protein interaction network analysis, transcriptomic validation, molecular docking, surface plasmon resonance (SPR), molecular dynamics simulation, and MM/PBSA analyses were performed to characterize representative target-compound interactions. Experimental validation to predict the therapeutic mechanism was performed using RAW264.7 macrophages, pulmonary artery smooth muscle cells (PASMCs), and a Sugen5416/hypoxia-induced murine model of PAH. A total of 67 overlapping therapeutic targets were identified, with enrichment analyses highlighting inflammation, oxidative stress, apoptosis, vascular remodeling, and the PI3K/AKT signaling pathway. AKT1 was identified as a central hub gene and was significantly upregulated under hypoxic conditions. Quercetin and Liquiritigenin (DFV)exhibited stable interactions with AKT1, with quercetin demonstrating stronger binding affinity (-11.10 kcal/mol) than liquiritigenin (-9.33 kcal/mol). Consistent with these computational predictions, Panax notoginseng reduced AKT1 expression and phosphorylation, attenuated oxidative stress and inflammatory cytokine production, inhibited PASMC proliferation and migration, and significantly improved pulmonary hemodynamics, right ventricular hypertrophy, and pulmonary vascular remodeling in vivo. Collectively, these findings identify AKT1 as a key molecular target through which Panax notoginseng exerts therapeutic effects against PAH in vivo.

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Cite

BibTeXRIS
BibTeX
@article{sheng2026integrated,
  title = {{Integrated Network Pharmacology and Experimental Validation Implicate AKT1‐Associated Signaling in the Protective Effects of Panax notoginseng Against Pulmonary Arterial Hypertension}},
  author = {YiFan Sheng and ZhiMeng Lu and TianYu Wang and HuiLin Tang and XinYao Liu and ZhiHao Zhao and Praise Audax Rukonge and GuiPing Yu},
  journal = {Pulmonary circulation},
  year = {2026},
  month = oct,
  doi = {10.1002/pul2.70435},
  url = {https://europepmc.org/article/PMC/PMC13717484},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Integrated Network Pharmacology and Experimental Validation Implicate AKT1‐Associated Signaling in the Protective Effects of Panax notoginseng Against Pulmonary Arterial Hypertension
AU  - YiFan Sheng
AU  - ZhiMeng Lu
AU  - TianYu Wang
AU  - HuiLin Tang
AU  - XinYao Liu
AU  - ZhiHao Zhao
AU  - Praise Audax Rukonge
AU  - GuiPing Yu
PY  - 2026
DA  - 2026/10/01
JO  - Pulmonary circulation
DO  - 10.1002/pul2.70435
UR  - https://europepmc.org/article/PMC/PMC13717484
AB  - Pulmonary arterial hypertension (PAH) is a progressive and fatal cardiopulmonary disease characterized by pulmonary vascular remodeling, endothelial dysfunction, inflammation, and increased pulmonary vascular resistance. Despite advances in targeted therapies, effective treatment options remain limited. This study investigated the molecular mechanisms underlying the therapeutic effects of Panax notoginseng against PAH through integrated computational and experimental validation. Network pharmacology was employed to identify the bioactive compounds and therapeutic targets of Panax notoginseng. Functional enrichment, protein-protein interaction network analysis, transcriptomic validation, molecular docking, surface plasmon resonance (SPR), molecular dynamics simulation, and MM/PBSA analyses were performed to characterize representative target-compound interactions. Experimental validation to predict the therapeutic mechanism was performed using RAW264.7 macrophages, pulmonary artery smooth muscle cells (PASMCs), and a Sugen5416/hypoxia-induced murine model of PAH. A total of 67 overlapping therapeutic targets were identified, with enrichment analyses highlighting inflammation, oxidative stress, apoptosis, vascular remodeling, and the PI3K/AKT signaling pathway. AKT1 was identified as a central hub gene and was significantly upregulated under hypoxic conditions. Quercetin and Liquiritigenin (DFV)exhibited stable interactions with AKT1, with quercetin demonstrating stronger binding affinity (-11.10 kcal/mol) than liquiritigenin (-9.33 kcal/mol). Consistent with these computational predictions, Panax notoginseng reduced AKT1 expression and phosphorylation, attenuated oxidative stress and inflammatory cytokine production, inhibited PASMC proliferation and migration, and significantly improved pulmonary hemodynamics, right ventricular hypertrophy, and pulmonary vascular remodeling in vivo. Collectively, these findings identify AKT1 as a key molecular target through which Panax notoginseng exerts therapeutic effects against PAH in vivo.
SN  - 2045-8932
SN  - 2045-8940
ER  -