Clinical and Translational Research
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Jun 26, 2024; 12(18): 3505-3514
Published online Jun 26, 2024. doi: 10.12998/wjcc.v12.i18.3505
Exploring the potential mechanism of WuFuYin against hypertrophic scar using network pharmacology and molecular docking
Shu-Yang Zhang, Song-Xue Guo, Lei-Lei Chen, Jia-Yan Zhu, Ming-Sheng Hou, Jia-Ke Lu, Xue-Xiang Shen
Shu-Yang Zhang, Jia-Yan Zhu, Xue-Xiang Shen, Department of General Surgery, Shaoxing Hospital of Traditional Chinese Medicine, Shaoxing 312000, Zhejiang Province, China
Song-Xue Guo, Department of Plastic Surgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China
Lei-Lei Chen, Hand and Plastic Surgery, The first People’s Hospital of Linping District, Hangzhou 311013, Zhejiang Province, China
Ming-Sheng Hou, Department of Pathology, Shaoxing Hospital of Traditional Chinese Medicine, Shaoxing 312000, Zhejiang Province, China
Jia-Ke Lu, Department of Traumatology, Yuyao Hospital of Traditional Chinese Medicine, Ningbo 315400, Zhejiang Province, China
Author contributions: Zhang SY, Guo SX, and Chen LL contributed to the conception and design; Zhang SY, Zhu JY, and Hou MS contributed to the collection and assembly of data; Lu JK and Shen XX analyzed and interpreted the data; and all authors wrote and approved the final manuscript.
Supported by the 2022 Shaoxing City Health Science and Technology Program (Health Science and Technology Program), No. 2022KY050.
Conflict-of-interest statement: There are no conflicts of interest to report.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xue-Xiang Shen, MD, Associate Chief Physician, Department of General Surgery, Shaoxing Hospital of Traditional Chinese Medicine, No. 641 Renmin Middle Road, Yuecheng District, Shaoxing 312000, Zhejiang Province, China. zsyzsy0522@163.com
Received: March 1, 2024
Revised: April 23, 2024
Accepted: April 30, 2024
Published online: June 26, 2024
Processing time: 109 Days and 1.1 Hours
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 CKD2, ABCC1, MMP2, MMP9, glycogen synthase kinase 3 beta (GSK3B), PRARG, MMP3, and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG) 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 GSK3B and 8-prenylated eriodictyol shared the highest affinity.

CONCLUSION

The current findings showed that the GSK3B and cyclin dependent kinase 2 were the potential targets and MOL004941, MOL004989, and MOL004993 were the main compounds of WFY in HTS treatment.

Keywords: WuFuYin; Hypertrophic scar; Network pharmacology; Molecular docking; Enrichment analysis

Core Tip: This study identified 8 hub genes [CKD2, ABCC1, MMP2, MMP9, glycogen synthase kinase 3 beta (GSK3B), PRARG, MMP3, and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG)] and five key compounds (MOL004941, MOL004935, MOL004866, MOL004993, and MOL004989) in the WuFuYin (WFY) as an effective treatment for hypertrophic scar (HTS). We found that PI3K-Akt pathway played a crucial role in the WFY. The results of molecular docking showed that GSK3B and cyclin dependent kinase 2 affected HTS through targeting MOL004941, MOL004989, and MOL004993.