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Autori principali: Liu, Zhi-Wen, Zhang, Bo-Bo, Kwok, Kevin Wing-Hin, Dong, Xiao-Li, Wong, Ka-Hing
Natura: Artículo científico
Lingua:en
Pubblicazione: International journal of molecular sciences 2025
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Accesso online:https://pubmed.ncbi.nlm.nih.gov/39940967/
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author Liu, Zhi-Wen
Zhang, Bo-Bo
Kwok, Kevin Wing-Hin
Dong, Xiao-Li
Wong, Ka-Hing
author_facet Liu, Zhi-Wen
Zhang, Bo-Bo
Kwok, Kevin Wing-Hin
Dong, Xiao-Li
Wong, Ka-Hing
Liu, Zhi-Wen
Zhang, Bo-Bo
Kwok, Kevin Wing-Hin
Dong, Xiao-Li
Wong, Ka-Hing
collection PubMed - marine biology
contents Network Pharmacology Analysis and Biological Validation Systemically Identified the Active Ingredients and Molecular Targets of Kudzu Root on Osteoporosis. Liu, Zhi-Wen Zhang, Bo-Bo Kwok, Kevin Wing-Hin Dong, Xiao-Li Wong, Ka-Hing Animals Zebrafish Network Pharmacology Pueraria Osteoporosis Molecular Docking Simulation Protein Interaction Maps Plant Roots Molecular Dynamics Simulation Signal Transduction Disease Models, Animal Plant Extracts Humans As a traditional medicinal food, Kudzu root (KR) has been proven to be an effective medicine for treating osteoporosis (OP). However, its precise targets and underlying integrated pharmacological mechanisms on OP have not yet been systematically investigated. The aim of the present study was to systemically explore the active ingredients, molecular targets, and ingredient-target network of KR against OP by the methods of network pharmacology followed by biological validation in a glucocorticoid-induced bone loss model of zebrafish. Our results identified a total of 15 active compounds with good pharmacokinetic properties in KR and 119 targets related to OP from correspondent databases, forming an ingredient-target network. Additionally, the protein-protein interaction (PPI) network further identified 39 core targets. Enrichment analyses with functional annotation revealed that the TNF signaling pathway and osteoclast differentiation process were significantly enriched by multi-targets including AKT1, P65, MAPK14, JUN, TNF-α, MMP9, IL6, and IL1B, etc., and served as the critical targets for molecular docking, molecular dynamics simulation, and in vivo experiment validation. These critical targets performed effectively in molecular docking and molecular dynamics, with AKT1, MMP9, and TNF-α exhibiting more prominent binding energy with Coumestrol, Genistein, and Genistein 7-glucoside, respectively. Further experimental validation in a zebrafish model indicated that KR could regulate the expressions of critical targets (AKT1, P65, MAPK14, JUN, TNF-α, and MMP9). This study provides a systemic perspective of the relationships between the active ingredients of KR and their multi-targets in OP, thereby constructing a pharmacological network to clarify the mechanisms by which KR ameliorates OP.
format Artículo científico
id pubmed_39940967
institution PubMed
language en
publishDate 2025
publisher International journal of molecular sciences
record_format pubmed
spellingShingle Network Pharmacology Analysis and Biological Validation Systemically Identified the Active Ingredients and Molecular Targets of Kudzu Root on Osteoporosis.
Liu, Zhi-Wen
Zhang, Bo-Bo
Kwok, Kevin Wing-Hin
Dong, Xiao-Li
Wong, Ka-Hing
Animals
Zebrafish
Network Pharmacology
Pueraria
Osteoporosis
Molecular Docking Simulation
Protein Interaction Maps
Plant Roots
Molecular Dynamics Simulation
Signal Transduction
Disease Models, Animal
Plant Extracts
Humans
Network Pharmacology Analysis and Biological Validation Systemically Identified the Active Ingredients and Molecular Targets of Kudzu Root on Osteoporosis. Liu, Zhi-Wen Zhang, Bo-Bo Kwok, Kevin Wing-Hin Dong, Xiao-Li Wong, Ka-Hing Animals Zebrafish Network Pharmacology Pueraria Osteoporosis Molecular Docking Simulation Protein Interaction Maps Plant Roots Molecular Dynamics Simulation Signal Transduction Disease Models, Animal Plant Extracts Humans As a traditional medicinal food, Kudzu root (KR) has been proven to be an effective medicine for treating osteoporosis (OP). However, its precise targets and underlying integrated pharmacological mechanisms on OP have not yet been systematically investigated. The aim of the present study was to systemically explore the active ingredients, molecular targets, and ingredient-target network of KR against OP by the methods of network pharmacology followed by biological validation in a glucocorticoid-induced bone loss model of zebrafish. Our results identified a total of 15 active compounds with good pharmacokinetic properties in KR and 119 targets related to OP from correspondent databases, forming an ingredient-target network. Additionally, the protein-protein interaction (PPI) network further identified 39 core targets. Enrichment analyses with functional annotation revealed that the TNF signaling pathway and osteoclast differentiation process were significantly enriched by multi-targets including AKT1, P65, MAPK14, JUN, TNF-α, MMP9, IL6, and IL1B, etc., and served as the critical targets for molecular docking, molecular dynamics simulation, and in vivo experiment validation. These critical targets performed effectively in molecular docking and molecular dynamics, with AKT1, MMP9, and TNF-α exhibiting more prominent binding energy with Coumestrol, Genistein, and Genistein 7-glucoside, respectively. Further experimental validation in a zebrafish model indicated that KR could regulate the expressions of critical targets (AKT1, P65, MAPK14, JUN, TNF-α, and MMP9). This study provides a systemic perspective of the relationships between the active ingredients of KR and their multi-targets in OP, thereby constructing a pharmacological network to clarify the mechanisms by which KR ameliorates OP.
title Network Pharmacology Analysis and Biological Validation Systemically Identified the Active Ingredients and Molecular Targets of Kudzu Root on Osteoporosis.
topic Animals
Zebrafish
Network Pharmacology
Pueraria
Osteoporosis
Molecular Docking Simulation
Protein Interaction Maps
Plant Roots
Molecular Dynamics Simulation
Signal Transduction
Disease Models, Animal
Plant Extracts
Humans
url https://pubmed.ncbi.nlm.nih.gov/39940967/