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Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation
by
Feng, Fanchao
, Zhou, Xianmei
, Xu, Yong
, Wang, Zhichao
, Qiu, Xirui
, Zhu, Dongwei
, Li, Tingyuan
, Pan, Tingyu
, Wu, Jieyu
, Wang, Jing
in
Actins - genetics
/ Actins - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Biomedicine
/ Bleomycin
/ Collagen (type I)
/ Collagen Type I - genetics
/ Collagen Type I - metabolism
/ Cyclooctanes - administration & dosage
/ Cyclooctanes - pharmacology
/ Cyclooctanes - therapeutic use
/ Disease Models, Animal
/ Fibroblasts - drug effects
/ Fibroblasts - metabolism
/ Fibrosis
/ Hypoxia-inducible factor 1a
/ Idiopathic Pulmonary Fibrosis - chemically induced
/ Idiopathic Pulmonary Fibrosis - drug therapy
/ Idiopathic Pulmonary Fibrosis - metabolism
/ Idiopathic Pulmonary Fibrosis - pathology
/ Immunofluorescence
/ Lignans - administration & dosage
/ Lignans - pharmacology
/ Lignans - therapeutic use
/ Lung - drug effects
/ Lung - metabolism
/ Lung - pathology
/ Lung diseases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Network Pharmacology
/ Neurosciences
/ NIH 3T3 Cells
/ Pharmacology/Toxicology
/ Polycyclic Compounds - administration & dosage
/ Polycyclic Compounds - pharmacology
/ Polycyclic Compounds - therapeutic use
/ Protein interaction
/ Protein Interaction Maps - drug effects
/ Pulmonary fibrosis
/ Signal transduction
/ Transforming Growth Factor beta - pharmacology
/ Transforming growth factor-b
2025
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Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation
by
Feng, Fanchao
, Zhou, Xianmei
, Xu, Yong
, Wang, Zhichao
, Qiu, Xirui
, Zhu, Dongwei
, Li, Tingyuan
, Pan, Tingyu
, Wu, Jieyu
, Wang, Jing
in
Actins - genetics
/ Actins - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Biomedicine
/ Bleomycin
/ Collagen (type I)
/ Collagen Type I - genetics
/ Collagen Type I - metabolism
/ Cyclooctanes - administration & dosage
/ Cyclooctanes - pharmacology
/ Cyclooctanes - therapeutic use
/ Disease Models, Animal
/ Fibroblasts - drug effects
/ Fibroblasts - metabolism
/ Fibrosis
/ Hypoxia-inducible factor 1a
/ Idiopathic Pulmonary Fibrosis - chemically induced
/ Idiopathic Pulmonary Fibrosis - drug therapy
/ Idiopathic Pulmonary Fibrosis - metabolism
/ Idiopathic Pulmonary Fibrosis - pathology
/ Immunofluorescence
/ Lignans - administration & dosage
/ Lignans - pharmacology
/ Lignans - therapeutic use
/ Lung - drug effects
/ Lung - metabolism
/ Lung - pathology
/ Lung diseases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Network Pharmacology
/ Neurosciences
/ NIH 3T3 Cells
/ Pharmacology/Toxicology
/ Polycyclic Compounds - administration & dosage
/ Polycyclic Compounds - pharmacology
/ Polycyclic Compounds - therapeutic use
/ Protein interaction
/ Protein Interaction Maps - drug effects
/ Pulmonary fibrosis
/ Signal transduction
/ Transforming Growth Factor beta - pharmacology
/ Transforming growth factor-b
2025
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Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation
by
Feng, Fanchao
, Zhou, Xianmei
, Xu, Yong
, Wang, Zhichao
, Qiu, Xirui
, Zhu, Dongwei
, Li, Tingyuan
, Pan, Tingyu
, Wu, Jieyu
, Wang, Jing
in
Actins - genetics
/ Actins - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Biomedicine
/ Bleomycin
/ Collagen (type I)
/ Collagen Type I - genetics
/ Collagen Type I - metabolism
/ Cyclooctanes - administration & dosage
/ Cyclooctanes - pharmacology
/ Cyclooctanes - therapeutic use
/ Disease Models, Animal
/ Fibroblasts - drug effects
/ Fibroblasts - metabolism
/ Fibrosis
/ Hypoxia-inducible factor 1a
/ Idiopathic Pulmonary Fibrosis - chemically induced
/ Idiopathic Pulmonary Fibrosis - drug therapy
/ Idiopathic Pulmonary Fibrosis - metabolism
/ Idiopathic Pulmonary Fibrosis - pathology
/ Immunofluorescence
/ Lignans - administration & dosage
/ Lignans - pharmacology
/ Lignans - therapeutic use
/ Lung - drug effects
/ Lung - metabolism
/ Lung - pathology
/ Lung diseases
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Network Pharmacology
/ Neurosciences
/ NIH 3T3 Cells
/ Pharmacology/Toxicology
/ Polycyclic Compounds - administration & dosage
/ Polycyclic Compounds - pharmacology
/ Polycyclic Compounds - therapeutic use
/ Protein interaction
/ Protein Interaction Maps - drug effects
/ Pulmonary fibrosis
/ Signal transduction
/ Transforming Growth Factor beta - pharmacology
/ Transforming growth factor-b
2025
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Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation
Journal Article
Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation
2025
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Overview
Idiopathic pulmonary fibrosis (IPF) is a worsening fibrotic condition characterized by a short survival rate and limited treatment options. This study evaluates the potential anti-fibrotic properties of Schisandrin B (Sch B) through network pharmacology and experimental validation. A mouse model of bleomycin-induced pulmonary fibrosis was established, and the modeled mice were treated with Sch B at three doses (20 mg/kg/day, 40 mg/kg/day, and 80 mg/kg/day). A fibrotic model was developed in NIH/3T3 cells by treating them with TGF-β (10 ng/mL) and administering Sch B at various concentrations (10, 20, and 40 µM). The results revealed that Sch B treatment delayed the development of bleomycin-induced pulmonary fibrosis and substantially decreased the transcription levels of collagen I and α-SMA in TGF-β-induced fibroblasts. Core targets were screened with protein-protein interaction network analysis, molecular complex detection (MCODE), and CytoHubba plugin. The application of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and molecular docking highlighted the significance of the HIF-1α signaling pathway in the potential mechanism of Sch B in IPF therapy. Western blot, PCR, and immunofluorescence were performed to validate the effects of Sch B on HIF-1α.
In vivo
and
in vitro
, Sch B administration reduced HIF-1α expression. These outcomes provide valuable insights into the potential mechanism by which Sch B delays IPF development, with HIF-1α potentially serving as a key target. However, further investigation is warranted to assess the safety and efficacy of Sch B in clinical settings.
Publisher
Springer Berlin Heidelberg,Springer Nature B.V
Subject
/ Animals
/ Biomedical and Life Sciences
/ Collagen Type I - metabolism
/ Cyclooctanes - administration & dosage
/ Cyclooctanes - therapeutic use
/ Fibrosis
/ Idiopathic Pulmonary Fibrosis - chemically induced
/ Idiopathic Pulmonary Fibrosis - drug therapy
/ Idiopathic Pulmonary Fibrosis - metabolism
/ Idiopathic Pulmonary Fibrosis - pathology
/ Lignans - administration & dosage
/ Male
/ Mice
/ Polycyclic Compounds - administration & dosage
/ Polycyclic Compounds - pharmacology
/ Polycyclic Compounds - therapeutic use
/ Protein Interaction Maps - drug effects
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