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加味二至丸促进雄激素性脱发毛发再生:基于网络药理学和分子对接技术探究其作用机制

Promotion of Hair Regrowth in Androgenetic Alopecia with Supplemented Erzhi Wan: Exploring Its Mechanism Using Network Pharmacology and Molecular Docking.

作者信息

Ji Chen, Ma Jun, Feng Chengcheng, Zhu Hongliu, Gao Yanwei, Huang Jun, Shen Hui, Wei Yuegang

机构信息

Department of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, People's Republic of China.

Department of Dermatology, the Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, People's Republic of China.

出版信息

Clin Cosmet Investig Dermatol. 2023 Oct 24;16:2995-3022. doi: 10.2147/CCID.S425295. eCollection 2023.

DOI:10.2147/CCID.S425295
PMID:37901149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10612515/
Abstract

PURPOSE

Supplemented Erzhi Wan (SEZW) is a Traditional Chinese Medicine commonly used in the treatment of androgenetic alopecia (AGA). This study aims to verify the effectiveness of SEZW for the treatment of AGA in mice and explore the potential molecular mechanisms underlying its function using network pharmacology and molecular docking.

METHODS

Forty mice were divided into five groups: Control, AGA-model, AGA-Positive, SEZW Low Dose, and SEZW High Dose. Hair regrowth in mice was evaluated by scoring hair on days 0, 14, and 28 post-treatment and weighing mouse hair on day 28 post-treatment. The targets of the active compounds of SEZW were obtained using the Traditional Chinese Medicine Database. AGA-related targets were downloaded from five databases. Then, the overlapping genes were identified. A protein-protein interaction network was constructed using the STRING database. Hub targets were determined through analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Finally, molecular docking of active compounds and hub targets was performed.

RESULTS

Hair regrowth in mice in the SEZW treatment groups was significantly enhanced relative to that in the AGA-model mice. A total of 59 potential drug-disease targets were identified. Based on the GO/KEGG analysis results, oxidative stress and gland development were identified as potential mechanisms of action of SEZW in AGA treatment. The PI3K-Akt and AGE-RAGE signaling pathways and seven hub targets were identified as the potential underlying mechanism of SEZW function. Molecular docking results showed that the most active SEZW compounds bind stably to several of the candidate disease targets.

CONCLUSION

SEZW is effective in the treatment of AGA in a mouse model. Combined with network pharmacological analysis, the potential mechanisms, signaling pathways, and hub targets of SEZW in the treatment of AGA were identified, providing new ideas for further studies.

摘要

目的

加味二至丸(SEZW)是一种常用于治疗雄激素性脱发(AGA)的中药。本研究旨在验证SEZW对小鼠AGA治疗的有效性,并利用网络药理学和分子对接探索其作用的潜在分子机制。

方法

将40只小鼠分为五组:对照组、AGA模型组、AGA阳性组、SEZW低剂量组和SEZW高剂量组。在治疗后第0、14和28天对小鼠毛发进行评分,并在治疗后第28天称量小鼠毛发重量,以评估小鼠毛发再生情况。利用中药数据库获取SEZW活性成分的靶点。从五个数据库下载AGA相关靶点。然后,鉴定重叠基因。使用STRING数据库构建蛋白质-蛋白质相互作用网络。通过分析确定枢纽靶点。进行基因本体(GO)和京都基因与基因组百科全书(KEGG)通路富集分析。最后,对活性成分和枢纽靶点进行分子对接。

结果

与AGA模型小鼠相比,SEZW治疗组小鼠的毛发再生明显增强。共鉴定出59个潜在的药物-疾病靶点。基于GO/KEGG分析结果,氧化应激和腺体发育被确定为SEZW治疗AGA的潜在作用机制。PI3K-Akt和AGE-RAGE信号通路以及七个枢纽靶点被确定为SEZW作用的潜在机制。分子对接结果表明,SEZW中最具活性化合物与几个候选疾病靶点稳定结合。

结论

SEZW对小鼠模型中的AGA治疗有效。结合网络药理学分析,确定了SEZW治疗AGA的潜在机制、信号通路和枢纽靶点,为进一步研究提供了新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/713c09679411/CCID-16-2995-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/36d6d65091f0/CCID-16-2995-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/e740d6074ab2/CCID-16-2995-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/ade82d8acf74/CCID-16-2995-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/0848674bf39a/CCID-16-2995-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/885c00790e1e/CCID-16-2995-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/713c09679411/CCID-16-2995-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/36d6d65091f0/CCID-16-2995-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/e740d6074ab2/CCID-16-2995-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/ade82d8acf74/CCID-16-2995-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/0848674bf39a/CCID-16-2995-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/885c00790e1e/CCID-16-2995-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a852/10612515/713c09679411/CCID-16-2995-g0006.jpg

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