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运用网络药理学和分子对接技术探索五倍饮治疗增生性瘢痕的潜在机制。

Exploring the potential mechanism of WuFuYin against hypertrophic scar using network pharmacology and molecular docking.

作者信息

Zhang Shu-Yang, Guo Song-Xue, Chen Lei-Lei, Zhu Jia-Yan, Hou Ming-Sheng, Lu Jia-Ke, Shen Xue-Xiang

机构信息

Department of General Surgery, Shaoxing Hospital of Traditional Chinese Medicine, Shaoxing 312000, Zhejiang Province, China.

Department of Plastic Surgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China.

出版信息

World J Clin Cases. 2024 Jun 26;12(18):3505-3514. doi: 10.12998/wjcc.v12.i18.3505.

DOI:10.12998/wjcc.v12.i18.3505
PMID:38983404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11229930/
Abstract

BACKGROUND: Hypertrophic scar (HTS) is dermal fibroproliferative disorder, which may cause physiological and psychological problems. Currently, the potential mechanism of WuFuYin (WFY) in the treatment of HTS remained to be elucidated. AIM: To explore the potential mechanism of WFY in treating HTS. METHODS: Active components and corresponding targets were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. HTS-related genes were obtained from the GeneCards, DisGeNET, and National Center for Biotechnology Information. The function of targets was analyzed by performing Gene Ontology and Kyoto Encyclopaedia of Genes and Genome (KEGG) enrichment analysis. A protein + IBM-protein interaction (PPI) network was developed using STRING database and Cytoscape. To confirm the high affinity between compounds and targets, molecular docking was performed. RESULTS: A total of 65 core genes, which were both related to compounds and HTS, were selected from multiple databases. PPI analysis showed that , , , , glycogen synthase kinase 3 beta (), , , and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma () were the hub targets and MOL004941, MOL004935, MOL004866, MOL004993, and MOL004989 were the key compounds of WFY against HTS. The results of KEGG enrichment analysis demonstrated that the function of most genes were enriched in the PI3K-Akt pathway. Moreover, by performing molecular docking, we confirmed that and 8-prenylated eriodictyol shared the highest affinity. CONCLUSION: The current findings showed that the and cyclin dependent kinase 2 were the potential targets and MOL004941, MOL004989, and MOL004993 were the main compounds of WFY in HTS treatment.

摘要

背景：增生性瘢痕（HTS）是一种真皮纤维增生性疾病，可导致生理和心理问题。目前，五倍子饮（WFY）治疗HTS的潜在机制仍有待阐明。 目的：探讨WFY治疗HTS的潜在机制。 方法：从中药系统药理学数据库及分析平台检索活性成分及相应靶点。从基因卡片、疾病基因数据库（DisGeNET）和美国国立生物技术信息中心获取HTS相关基因。通过基因本体论（Gene Ontology）和京都基因与基因组百科全书（KEGG）富集分析对靶点功能进行分析。利用STRING数据库和Cytoscape构建蛋白质-蛋白质相互作用（PPI）网络。为证实化合物与靶点之间的高亲和力，进行分子对接。 结果：从多个数据库中筛选出65个与化合物和HTS均相关的核心基因。PPI分析表明，[此处原文缺失具体基因名称]、糖原合酶激酶3β（[此处原文缺失具体基因名称]）、磷脂酰肌醇-4,5-二磷酸3-激酶催化亚基γ（[此处原文缺失具体基因名称]）是核心靶点，MOL004941、MOL004935、MOL004866、MOL004993和MOL004989是WFY抗HTS的关键化合物。KEGG富集分析结果表明，大多数基因的功能富集于PI3K-Akt信号通路。此外，通过分子对接，我们证实[此处原文缺失具体化合物名称]与8-异戊烯基圣草酚具有最高亲和力。 结论：目前的研究结果表明，[此处原文缺失具体基因名称]和细胞周期蛋白依赖性激酶2是潜在靶点，MOL004941、MOL004989和MOL004993是WFY治疗HTS的主要化合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/b0d95832f9b3/WJCC-12-3505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/b352938be943/WJCC-12-3505-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/51520de42dd9/WJCC-12-3505-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/549effd83523/WJCC-12-3505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/a640779e4026/WJCC-12-3505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/0ca00138fecc/WJCC-12-3505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/b0d95832f9b3/WJCC-12-3505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/b352938be943/WJCC-12-3505-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/51520de42dd9/WJCC-12-3505-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/549effd83523/WJCC-12-3505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/a640779e4026/WJCC-12-3505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/0ca00138fecc/WJCC-12-3505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b718/11229930/b0d95832f9b3/WJCC-12-3505-g006.jpg

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本文引用的文献

[1]
Identification of PIK3CG as a hub in septic myocardial injury using network pharmacology and weighted gene co-expression network analysis.

Bioeng Transl Med. 2022-8-3

[2]
The Role of Local Inflammation and Hypoxia in the Formation of Hypertrophic Scars-A New Model in the Duroc Pig.

Int J Mol Sci. 2022-12-24

[3]
A novel lncRNA FPASL regulates fibroblast proliferation via the PI3K/AKT and MAPK signaling pathways in hypertrophic scar.

Acta Biochim Biophys Sin (Shanghai). 2022-9-25

[4]
KLF4 Alleviates Hypertrophic Scar Fibrosis by Directly Activating BMP4 Transcription.

Int J Biol Sci. 2022

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The licorice flavonoid isoliquiritigenin attenuates Mycobacterium tuberculosis-induced inflammation through Notch1/NF-κB and MAPK signaling pathways.

J Ethnopharmacol. 2022-8-10

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Ginseng root extract attenuates inflammation by inhibiting the MAPK/NF-κB signaling pathway and activating autophagy and p62-Nrf2-Keap1 signaling in vitro and in vivo.

J Ethnopharmacol. 2022-1-30

[8]
Strategies to Overcome Failures in T-Cell Immunotherapies by Targeting PI3K-δ and -γ.

Front Immunol. 2021

[9]
Polysaccharide of Atractylodes macrocephala Koidz regulates LPS-mediated mouse hepatitis through the TLR4-MyD88-NFκB signaling pathway.

Int Immunopharmacol. 2021-9

[10]
Glycogen Synthase Kinase 3β Modulates the Inflammatory Response Activated by Bacteria, Viruses, and Parasites.

Front Immunol. 2021

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