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Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network

Pulmonary fibrosis is a chronic, progressive and irreversible heterogeneous disease of pulmonary interstitial tissue. Its incidence is increasing year by year in the world, and it will be further increased due to the pandemic of COVID-19. However, at present, there is no safe and effective treatment...

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Autores principales: Bing, Pingping, Zhou, Wenhu, Tan, Songwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8964346/
https://www.ncbi.nlm.nih.gov/pubmed/35370663
http://dx.doi.org/10.3389/fphar.2022.865065
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author Bing, Pingping
Zhou, Wenhu
Tan, Songwen
author_facet Bing, Pingping
Zhou, Wenhu
Tan, Songwen
author_sort Bing, Pingping
collection PubMed
description Pulmonary fibrosis is a chronic, progressive and irreversible heterogeneous disease of pulmonary interstitial tissue. Its incidence is increasing year by year in the world, and it will be further increased due to the pandemic of COVID-19. However, at present, there is no safe and effective treatment for this disease, so it is very meaningful to find drugs with high efficiency and less adverse reactions. The natural astragalus polysaccharide has the pharmacological effect of anti-pulmonary fibrosis with little toxic and side effects. At present, the mechanism of anti-pulmonary fibrosis of astragalus polysaccharide is not clear. Based on the network pharmacology and molecular docking method, this study analyzes the mechanism of Astragalus polysaccharides in treating pulmonary fibrosis, which provides a theoretical basis for its further clinical application. The active components of Astragalus polysaccharides were screened out by Swisstarget database, and the related targets of pulmonary fibrosis were screened out by GeneCards database. Protein-protein interaction network analysis and molecular docking were carried out to verify the docking affinity of active ingredients. At present, through screening, we have obtained 92 potential targets of Astragalus polysaccharides for treating pulmonary fibrosis, including 11 core targets. Astragalus polysaccharides has the characteristics of multi-targets and multi-pathways, and its mechanism of action may be through regulating the expression of VCAM1, RELA, CDK2, JUN, CDK1, HSP90AA1, NOS2, SOD1, CASP3, AHSA1, PTGER3 and other genes during the development of pulmonary fibrosis.
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spelling pubmed-89643462022-03-31 Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network Bing, Pingping Zhou, Wenhu Tan, Songwen Front Pharmacol Pharmacology Pulmonary fibrosis is a chronic, progressive and irreversible heterogeneous disease of pulmonary interstitial tissue. Its incidence is increasing year by year in the world, and it will be further increased due to the pandemic of COVID-19. However, at present, there is no safe and effective treatment for this disease, so it is very meaningful to find drugs with high efficiency and less adverse reactions. The natural astragalus polysaccharide has the pharmacological effect of anti-pulmonary fibrosis with little toxic and side effects. At present, the mechanism of anti-pulmonary fibrosis of astragalus polysaccharide is not clear. Based on the network pharmacology and molecular docking method, this study analyzes the mechanism of Astragalus polysaccharides in treating pulmonary fibrosis, which provides a theoretical basis for its further clinical application. The active components of Astragalus polysaccharides were screened out by Swisstarget database, and the related targets of pulmonary fibrosis were screened out by GeneCards database. Protein-protein interaction network analysis and molecular docking were carried out to verify the docking affinity of active ingredients. At present, through screening, we have obtained 92 potential targets of Astragalus polysaccharides for treating pulmonary fibrosis, including 11 core targets. Astragalus polysaccharides has the characteristics of multi-targets and multi-pathways, and its mechanism of action may be through regulating the expression of VCAM1, RELA, CDK2, JUN, CDK1, HSP90AA1, NOS2, SOD1, CASP3, AHSA1, PTGER3 and other genes during the development of pulmonary fibrosis. Frontiers Media S.A. 2022-03-08 /pmc/articles/PMC8964346/ /pubmed/35370663 http://dx.doi.org/10.3389/fphar.2022.865065 Text en Copyright © 2022 Bing, Zhou and Tan. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Bing, Pingping
Zhou, Wenhu
Tan, Songwen
Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title_full Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title_fullStr Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title_full_unstemmed Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title_short Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on “Drug-Target-Pathway” Network
title_sort study on the mechanism of astragalus polysaccharide in treating pulmonary fibrosis based on “drug-target-pathway” network
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8964346/
https://www.ncbi.nlm.nih.gov/pubmed/35370663
http://dx.doi.org/10.3389/fphar.2022.865065
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