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基于网络药理学对一贯煎治疗慢性肝炎关键机制的分析

Network pharmacology-based analysis on the key mechanisms of Yiguanjian acting on chronic hepatitis.

作者信息

Jiang Xiaodan, Cui Xinyi, Nie Ruifang, You Hongjie, Tang Zuoqing, Liu Wenlan

机构信息

School of Traditional Chinese Medicine, Capital Medical University, Beijing, China.

School of Basic Medical Sciences, Capital Medical University, Beijing, China.

出版信息

Heliyon. 2024 May 1;10(9):e29977. doi: 10.1016/j.heliyon.2024.e29977. eCollection 2024 May 15.

DOI:10.1016/j.heliyon.2024.e29977
PMID:38756592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11096846/
Abstract

Chronic hepatitis (CH) encompasses a prevalent array of liver conditions that significantly contribute to global morbidity and mortality. Yiguanjian (YGJ) is a classical traditional Chinese medicine with a long history of medicinal as a treatment for CH. Although it has been reported that YGJ can reduce liver inflammation, the intricate mechanism requires further elucidation. We used network pharmacology approaches in this work, such as gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and network-based analysis of protein-protein interactions (PPIs), to clarify the pharmacological constituents, potential therapeutic targets, and YGJ signaling pathways associated with CH. Employing the random walk restart (RWR) algorithm, we identified GNAS, GNB1, CYP2E1, SFTPC, F2, MAPK3, PLG, SRC, HDAC1, and STAT3 as pivotal targets within the PPI network of YGJ-CH. YGJ attenuated liver inflammation and inhibited GNAS/STAT3 signaling . , we overexpressed the gene further to verify the critical role of GNAS in YGJ treatment. Our findings highlight GNAS/STAT3 as a promising therapeutic target for CH, providing a basis and direction for future investigations.

摘要

慢性肝炎(CH)涵盖了一系列常见的肝脏疾病,这些疾病对全球发病率和死亡率有显著影响。一贯煎(YGJ)是一种经典的传统中药,作为治疗CH已有悠久的药用历史。虽然已有报道称YGJ可减轻肝脏炎症,但其复杂机制仍需进一步阐明。在这项工作中,我们采用网络药理学方法,如基因本体(GO)分析、京都基因与基因组百科全书(KEGG)分析以及基于网络的蛋白质-蛋白质相互作用(PPI)分析,以阐明与CH相关的YGJ的药理成分、潜在治疗靶点和信号通路。利用随机游走重启(RWR)算法,我们在YGJ-CH的PPI网络中确定GNAS、GNB1、CYP2E1、SFTPC、F2、MAPK3、PLG、SRC、HDAC1和STAT3为关键靶点。YGJ减轻了肝脏炎症并抑制了GNAS/STAT3信号传导。此外,我们进一步过表达该基因以验证GNAS在YGJ治疗中的关键作用。我们的研究结果突出了GNAS/STAT3作为CH的一个有前景的治疗靶点,为未来的研究提供了基础和方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/9b40a9ce2d61/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/98ee32132510/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/9821313454de/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/e1e9ebbd2348/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/c78850c23db3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/9b40a9ce2d61/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/047aa9adb89b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/579e5cf53d03/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/98ee32132510/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/9821313454de/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/e1e9ebbd2348/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/c78850c23db3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28af/11096846/9b40a9ce2d61/gr7.jpg

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