Exploring the mechanism of Cassiae semen in regulating lipid metabolism through network pharmacology and experimental validation

Multiple studies have assessed the role of Cassiae semen (CS) in regulating lipid metabolism. However, the mechanism of action of CS on non-alcoholic fatty liver disease (NAFLD) has seen rare scrutiny. The objective of this study was to explore the regulatory mechanism of CS on lipid metabolism in N...

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Published in:Bioscience reports 2023-02, Vol.43 (2), p.1
Main Authors: Huang, Lili, Zhu, Haiyan, Tang, Yuqin, Luo, Zheng, Xia, Luyun, Zhang, Chunjiang, Wang, Yanqiu, Huai, Wenying, Fang, Zhiyan, Li, Shenrong, Yan, Zhiyong, Yin, Qiaozhi, Zhang, Tian-E
Format: Article
Language:English
Subjects:
Accumulation
Amyloid beta-Peptides
Amyloid precursor protein
Bioinformatics
Caspase 3
Chinese medicine
Class I Phosphatidylinositol 3-Kinases
Down-regulation
Drugs, Chinese Herbal - pharmacology
Epidermal growth factor receptors
ErbB Receptors
Ethanol
Fatty liver
Genes
Growth factors
Herbal medicine
Humans
Hyperlipidemia
Intracellular signalling
Kinases
Lipid Metabolism
Lipids
Liver diseases
MAP kinase
Medical research
Metabolism
Molecular Bases of Health & Disease
Molecular docking
Molecular Docking Simulation
Network Pharmacology
Non-alcoholic Fatty Liver Disease - drug therapy
Non-alcoholic Fatty Liver Disease - genetics
Pharmacology
Phosphatidylinositol 4,5-diphosphate
Plant extracts
Proteins
Quinizarin
R&D
Regulatory mechanisms (biology)
Research & development
Seeds
Signal transduction
Signaling
Software
Therapeutic targets
Traditional Chinese medicine
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cited_by cdi_FETCH-LOGICAL-c437t-5bc545329a4d30623631f2f295d5706576bd28646bdb4f4e756e9ec79f2dd6263
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container_issue 2
container_start_page 1
container_title Bioscience reports
container_volume 43
creator Huang, Lili
Zhu, Haiyan
Tang, Yuqin
Luo, Zheng
Xia, Luyun
Zhang, Chunjiang
Wang, Yanqiu
Huai, Wenying
Fang, Zhiyan
Li, Shenrong
Yan, Zhiyong
Yin, Qiaozhi
Zhang, Tian-E
description Multiple studies have assessed the role of Cassiae semen (CS) in regulating lipid metabolism. However, the mechanism of action of CS on non-alcoholic fatty liver disease (NAFLD) has seen rare scrutiny. The objective of this study was to explore the regulatory mechanism of CS on lipid metabolism in NAFLD. Components of CS ethanol extract (CSEE) were analyzed and identified using UPLC-Q-Orbirap HRMS. The candidate compounds of CS and its relative targets were extracted from the Traditional Chinese Medicine Systems Pharmacology, Swiss-Target-Prediction, and TargetNet web server. The Therapeutic Target Database, Genecards, Online Mendelian Inheritance in Man, and DisGeNET were searched for NAFLD targets. Binding affinity between potential core components and key targets was established employing molecular docking simulations. After that, free fatty acid (FFA)-induced HepG2 cells were used to further validate part of the network pharmacology results. Six genes, including Caspase 3 (CASP3), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA), epidermal growth factor receptor (EGFR), and amyloid β (A4) precursor protein (APP) were identified as key targets. The mitogen-activated protein kinase (MAPK) signaling pathway was found to associate closely with CS's effect on NAFLD. Per molecular docking findings, toralactone and quinizarin formed the most stable combinations with hub genes. About 0.1 (vs. FFA, P
doi_str_mv 10.1042/BSR20221375
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However, the mechanism of action of CS on non-alcoholic fatty liver disease (NAFLD) has seen rare scrutiny. The objective of this study was to explore the regulatory mechanism of CS on lipid metabolism in NAFLD. Components of CS ethanol extract (CSEE) were analyzed and identified using UPLC-Q-Orbirap HRMS. The candidate compounds of CS and its relative targets were extracted from the Traditional Chinese Medicine Systems Pharmacology, Swiss-Target-Prediction, and TargetNet web server. The Therapeutic Target Database, Genecards, Online Mendelian Inheritance in Man, and DisGeNET were searched for NAFLD targets. Binding affinity between potential core components and key targets was established employing molecular docking simulations. After that, free fatty acid (FFA)-induced HepG2 cells were used to further validate part of the network pharmacology results. Six genes, including Caspase 3 (CASP3), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA), epidermal growth factor receptor (EGFR), and amyloid β (A4) precursor protein (APP) were identified as key targets. The mitogen-activated protein kinase (MAPK) signaling pathway was found to associate closely with CS's effect on NAFLD. Per molecular docking findings, toralactone and quinizarin formed the most stable combinations with hub genes. About 0.1 (vs. FFA, P&lt;0.01) and 0.2 (vs. FFA, P&lt;0.05) mg/ml CSEE decreased lipid accumulation in vitro by reversing the up-regulation of CASP3, EGFR, and APP and the down-regulation of PIK3CA. 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Disease</topic><topic>Molecular docking</topic><topic>Molecular Docking Simulation</topic><topic>Network Pharmacology</topic><topic>Non-alcoholic Fatty Liver Disease - drug therapy</topic><topic>Non-alcoholic Fatty Liver Disease - genetics</topic><topic>Pharmacology</topic><topic>Phosphatidylinositol 4,5-diphosphate</topic><topic>Plant extracts</topic><topic>Proteins</topic><topic>Quinizarin</topic><topic>R&amp;D</topic><topic>Regulatory mechanisms (biology)</topic><topic>Research &amp; development</topic><topic>Seeds</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Software</topic><topic>Therapeutic targets</topic><topic>Traditional Chinese medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Lili</creatorcontrib><creatorcontrib>Zhu, Haiyan</creatorcontrib><creatorcontrib>Tang, Yuqin</creatorcontrib><creatorcontrib>Luo, Zheng</creatorcontrib><creatorcontrib>Xia, Luyun</creatorcontrib><creatorcontrib>Zhang, Chunjiang</creatorcontrib><creatorcontrib>Wang, Yanqiu</creatorcontrib><creatorcontrib>Huai, Wenying</creatorcontrib><creatorcontrib>Fang, Zhiyan</creatorcontrib><creatorcontrib>Li, Shenrong</creatorcontrib><creatorcontrib>Yan, Zhiyong</creatorcontrib><creatorcontrib>Yin, Qiaozhi</creatorcontrib><creatorcontrib>Zhang, Tian-E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health &amp; 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However, the mechanism of action of CS on non-alcoholic fatty liver disease (NAFLD) has seen rare scrutiny. The objective of this study was to explore the regulatory mechanism of CS on lipid metabolism in NAFLD. Components of CS ethanol extract (CSEE) were analyzed and identified using UPLC-Q-Orbirap HRMS. The candidate compounds of CS and its relative targets were extracted from the Traditional Chinese Medicine Systems Pharmacology, Swiss-Target-Prediction, and TargetNet web server. The Therapeutic Target Database, Genecards, Online Mendelian Inheritance in Man, and DisGeNET were searched for NAFLD targets. Binding affinity between potential core components and key targets was established employing molecular docking simulations. After that, free fatty acid (FFA)-induced HepG2 cells were used to further validate part of the network pharmacology results. Six genes, including Caspase 3 (CASP3), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA), epidermal growth factor receptor (EGFR), and amyloid β (A4) precursor protein (APP) were identified as key targets. The mitogen-activated protein kinase (MAPK) signaling pathway was found to associate closely with CS's effect on NAFLD. Per molecular docking findings, toralactone and quinizarin formed the most stable combinations with hub genes. About 0.1 (vs. FFA, P&lt;0.01) and 0.2 (vs. FFA, P&lt;0.05) mg/ml CSEE decreased lipid accumulation in vitro by reversing the up-regulation of CASP3, EGFR, and APP and the down-regulation of PIK3CA. CSEE can significantly reduce intracellular lipid accumulation by modulating the MAPK signaling pathway to decrease CASP3 and EGFR expression.</abstract><cop>England</cop><pub>Portland Press Ltd The Biochemical Society</pub><pmid>36645186</pmid><doi>10.1042/BSR20221375</doi><orcidid>https://orcid.org/0000-0002-1081-5532</orcidid><orcidid>https://orcid.org/0000-0002-6395-4747</orcidid><oa>free_for_read</oa></addata></record>
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subjects Accumulation
Amyloid beta-Peptides
Amyloid precursor protein
Bioinformatics
Caspase 3
Chinese medicine
Class I Phosphatidylinositol 3-Kinases
Down-regulation
Drugs, Chinese Herbal - pharmacology
Epidermal growth factor receptors
ErbB Receptors
Ethanol
Fatty liver
Genes
Growth factors
Herbal medicine
Humans
Hyperlipidemia
Intracellular signalling
Kinases
Lipid Metabolism
Lipids
Liver diseases
MAP kinase
Medical research
Metabolism
Molecular Bases of Health & Disease
Molecular docking
Molecular Docking Simulation
Network Pharmacology
Non-alcoholic Fatty Liver Disease - drug therapy
Non-alcoholic Fatty Liver Disease - genetics
Pharmacology
Phosphatidylinositol 4,5-diphosphate
Plant extracts
Proteins
Quinizarin
R&D
Regulatory mechanisms (biology)
Research & development
Seeds
Signal transduction
Signaling
Software
Therapeutic targets
Traditional Chinese medicine
title Exploring the mechanism of Cassiae semen in regulating lipid metabolism through network pharmacology and experimental validation
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