Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with high incidence, morbidity, and mortality rates. Jinshui Huanxian formula (JHF) is an empirical formula that targets the pathogenesis of lung-kidney qi deficiency and phlegm-blood stasis in pulmonary fibrosis (PF). The purpose...

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Main Authors: Tiantian Liu, Pengli Xu, Shuishui Qi, Shaorui Ke, Qin Hu, Peng Zhao, Jiansheng Li
Format: Article
Language:English
Published: Hindawi Limited 2021-01-01
Series:Evidence-Based Complementary and Alternative Medicine
Online Access:http://dx.doi.org/10.1155/2021/8634705
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spelling doaj-ef18336265ea4594acc58f4f943140212021-07-19T01:04:22ZengHindawi LimitedEvidence-Based Complementary and Alternative Medicine1741-42882021-01-01202110.1155/2021/8634705Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary FibrosisTiantian Liu0Pengli Xu1Shuishui Qi2Shaorui Ke3Qin Hu4Peng Zhao5Jiansheng Li6Henan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseHenan Key Laboratory of Chinese Medicine for Respiratory DiseaseIdiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with high incidence, morbidity, and mortality rates. Jinshui Huanxian formula (JHF) is an empirical formula that targets the pathogenesis of lung-kidney qi deficiency and phlegm-blood stasis in pulmonary fibrosis (PF). The purpose of this study was to explore JHF’s potential pharmacological mechanisms in IPF therapy using network intersection analysis. JHF’s primary active components and corresponding target genes were predicted using various databases. Two sets of IPF disease genes were obtained from the DisGeNET and GEO databases and two sets of IPF drug targets were collected. The disease and drug target genes were analyzed. The JHF target genes that intersected with IPF’s differentially expressed genes were identified to predict JHF’s targets of action in IPF. The functions and pathways of predicted targets acting on IPF were analyzed using the DAVID and KEGG pathway databases. Finally, the resulting drug target mechanisms were validated in a rat model of PF. The initial analyses identified 494 active compounds and 1,304 corresponding targets for JHF. The intersection analysis revealed four common genes for the JHF targets, IPF disease, and anti-IPF drugs in the KEGG database. Furthermore, these genes were targeted by several JHF compounds. Seventy-two JHF targets were closely related to IPF, which suggests that they are therapeutically relevant. Target screening revealed that they regulate IPF through 18 pathways. The targets’ molecular functions included regulation of oxidoreductase activity, kinase regulator activity, phosphotransferase activity, and transmembrane receptor protein kinase activity. In vivo experiments showed that JHF alleviated the degree of PF, including decreases in collagen deposition and epithelial-mesenchymal transition. This study systematically explored JHF’s mechanisms to identify the specific target pathways involved in IPF. The generated pharmacological network, paired with in vivo validation, elucidates the potential roles and mechanisms of JHF in IPF therapy.http://dx.doi.org/10.1155/2021/8634705
collection DOAJ
language English
format Article
sources DOAJ
author Tiantian Liu
Pengli Xu
Shuishui Qi
Shaorui Ke
Qin Hu
Peng Zhao
Jiansheng Li
spellingShingle Tiantian Liu
Pengli Xu
Shuishui Qi
Shaorui Ke
Qin Hu
Peng Zhao
Jiansheng Li
Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
Evidence-Based Complementary and Alternative Medicine
author_facet Tiantian Liu
Pengli Xu
Shuishui Qi
Shaorui Ke
Qin Hu
Peng Zhao
Jiansheng Li
author_sort Tiantian Liu
title Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
title_short Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
title_full Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
title_fullStr Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
title_full_unstemmed Network Pharmacology-Based Mechanistic Investigation of Jinshui Huanxian Formula Acting on Idiopathic Pulmonary Fibrosis
title_sort network pharmacology-based mechanistic investigation of jinshui huanxian formula acting on idiopathic pulmonary fibrosis
publisher Hindawi Limited
series Evidence-Based Complementary and Alternative Medicine
issn 1741-4288
publishDate 2021-01-01
description Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with high incidence, morbidity, and mortality rates. Jinshui Huanxian formula (JHF) is an empirical formula that targets the pathogenesis of lung-kidney qi deficiency and phlegm-blood stasis in pulmonary fibrosis (PF). The purpose of this study was to explore JHF’s potential pharmacological mechanisms in IPF therapy using network intersection analysis. JHF’s primary active components and corresponding target genes were predicted using various databases. Two sets of IPF disease genes were obtained from the DisGeNET and GEO databases and two sets of IPF drug targets were collected. The disease and drug target genes were analyzed. The JHF target genes that intersected with IPF’s differentially expressed genes were identified to predict JHF’s targets of action in IPF. The functions and pathways of predicted targets acting on IPF were analyzed using the DAVID and KEGG pathway databases. Finally, the resulting drug target mechanisms were validated in a rat model of PF. The initial analyses identified 494 active compounds and 1,304 corresponding targets for JHF. The intersection analysis revealed four common genes for the JHF targets, IPF disease, and anti-IPF drugs in the KEGG database. Furthermore, these genes were targeted by several JHF compounds. Seventy-two JHF targets were closely related to IPF, which suggests that they are therapeutically relevant. Target screening revealed that they regulate IPF through 18 pathways. The targets’ molecular functions included regulation of oxidoreductase activity, kinase regulator activity, phosphotransferase activity, and transmembrane receptor protein kinase activity. In vivo experiments showed that JHF alleviated the degree of PF, including decreases in collagen deposition and epithelial-mesenchymal transition. This study systematically explored JHF’s mechanisms to identify the specific target pathways involved in IPF. The generated pharmacological network, paired with in vivo validation, elucidates the potential roles and mechanisms of JHF in IPF therapy.
url http://dx.doi.org/10.1155/2021/8634705
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