Novel molecular mechanisms of eosinophil-mediated chronic obstructive pulmonary disease induced by bezo[a]pyrene

This study aimed to explore molecular mechanisms of benzo[a]pyrene (B[a]P) induced eosinophil-associated chronic obstructive pulmonary disease (COPD) via network toxicology and molecular dynamics modeling. Analyze chemical structures using PubChem, integrate STITCH, Swiss Target Prediction and ChEMBL databases to predict potential target molecules; use ADMETlab to assess physicochemical properties and PROTOX to predict toxicity; combine STRING and Cytoscape (based on UniProt data standardization) to screen core disease-related target molecules; conduct Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, focusing on inflammation and immune regulation pathways; perform molecular docking using AutoDock; visualize key binding sites using PyMOL/Discovery Studio; conduct 100-ns molecular dynamics simulations using Gromacs; and systematically assess the stability and dynamic mechanisms of the B[a]P-target complex based on root-mean-square deviation (RMSD) fluctuations and changes in radius of gyration. This study screened 48 potential targets related to eosinophils in COPD through protein interaction analysis, focusing on five core targets: PTPRC, SRC, AKT1, MYC, and CSF-1R. GO and KEGG analyses revealed their involvement in inflammation- and immune-related biological processes and signaling pathways. Molecular docking and kinetic simulations confirmed stable binding between the targets and B[a]P, with PTPRC exhibiting exceptionally high stability in its interactions. This study elucidated the molecular mechanisms underlying B[a]P-induced eosinophil-related COPD through network toxicology, molecular docking and kinetic modeling. It identified key targets (PTPRC, AKT1, CSF-1R) and elucidated the molecular mechanisms linking environmental pollutants to COPD pathology and the association between environmental pollutants and eosinophil-associated COPD pathology. These findings provide a scientific basis for targeted interventions.

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Publication Details

Journal
Clinical and Experimental Medicine
Published
2025-11-06
DOI
https://doi.org/10.1007/s10238-025-01901-x
Primary Topic
Chronic Obstructive Pulmonary Disease (COPD) Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Novel molecular mechanisms of eosinophil-mediated chronic obstructive pulmonary disease induced by bezo[a]pyrene

Chengyu Jiao, Shihuan Yu, Xinyi Wang, Lu Liu et al.
Clinical and Experimental Medicine
Chronic Obstructive Pulmonary Disease (COPD) Research
article

Novel molecular mechanisms of eosinophil-mediated chronic obstructive pulmonary disease induced by bezo[a]pyrene

Chengyu Jiao, Shihuan Yu, Xinyi Wang, Lu Liu, Chunling Zhang, Jinling Xiao, Hang Liu
article en

Abstract

This study aimed to explore molecular mechanisms of benzo[a]pyrene (B[a]P) induced eosinophil-associated chronic obstructive pulmonary disease (COPD) via network toxicology and molecular dynamics modeling. Analyze chemical structures using PubChem, integrate STITCH, Swiss Target Prediction and ChEMBL databases to predict potential target molecules; use ADMETlab to assess physicochemical properties and PROTOX to predict toxicity; combine STRING and Cytoscape (based on UniProt data standardization) to screen core disease-related target molecules; conduct Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, focusing on inflammation and immune regulation pathways; perform molecular docking using AutoDock; visualize key binding sites using PyMOL/Discovery Studio; conduct 100-ns molecular dynamics simulations using Gromacs; and systematically assess the stability and dynamic mechanisms of the B[a]P-target complex based on root-mean-square deviation (RMSD) fluctuations and changes in radius of gyration. This study screened 48 potential targets related to eosinophils in COPD through protein interaction analysis, focusing on five core targets: PTPRC, SRC, AKT1, MYC, and CSF-1R. GO and KEGG analyses revealed their involvement in inflammation- and immune-related biological processes and signaling pathways. Molecular docking and kinetic simulations confirmed stable binding between the targets and B[a]P, with PTPRC exhibiting exceptionally high stability in its interactions. This study elucidated the molecular mechanisms underlying B[a]P-induced eosinophil-related COPD through network toxicology, molecular docking and kinetic modeling. It identified key targets (PTPRC, AKT1, CSF-1R) and elucidated the molecular mechanisms linking environmental pollutants to COPD pathology and the association between environmental pollutants and eosinophil-associated COPD pathology. These findings provide a scientific basis for targeted interventions.

Clinical and Experimental MedicineVol. 25(1)
Harbin Medical University (CN), First Affiliated Hospital of Harbin Medical University (CN)
Harbin Medical University
Openalex Percentile: Top 53%
Chronic Obstructive Pulmonary Disease (COPD) Research
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