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基于网络药理学揭示中药FDY2004的抗肺癌机制

Uncovering the Anti-Lung-Cancer Mechanisms of the Herbal Drug FDY2004 by Network Pharmacology.

作者信息

Lee Ho-Sung, Lee In-Hee, Kang Kyungrae, Park Sang-In, Kwon Tae-Wook, Lee Dae-Yeon

机构信息

The Fore, 87 Ogeum-ro, Songpa-gu, Seoul 05542, Republic of Korea.

Forest Hospital, 129 Ogeum-ro, Songpa-gu, Seoul 05549, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2021 Feb 4;2021:6644018. doi: 10.1155/2021/6644018. eCollection 2021.

DOI:10.1155/2021/6644018
PMID:33628308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7886515/
Abstract

With growing evidence on the therapeutic efficacy and safety of herbal drugs, there has been a substantial increase in their application in the lung cancer treatment. Meanwhile, their action mechanisms at the system level have not been comprehensively uncovered. To this end, we employed a network pharmacology methodology to elucidate the systematic action mechanisms of FDY2004, an anticancer herbal drug composed of Moutan Radicis Cortex, Persicae Semen, and Rhei Radix et Rhizoma, in lung cancer treatment. By evaluating the pharmacokinetic properties of the chemical compounds present in FDY2004 using herbal medicine-associated databases, we identified its 29 active chemical components interacting with 141 lung cancer-associated therapeutic targets in humans. The functional enrichment analysis of the lung cancer-related targets of FDY2004 revealed the enriched Gene Ontology terms, involving the regulation of cell proliferation and growth, cell survival and death, and oxidative stress responses. Moreover, we identified key FDY2004-targeted oncogenic and tumor-suppressive pathways associated with lung cancer, including the phosphatidylinositol 3-kinase-Akt, mitogen-activated protein kinase, tumor necrosis factor, Ras, focal adhesion, and hypoxia-inducible factor-1 signaling pathways. Overall, our study provides novel evidence and basis for research on the comprehensive anticancer mechanisms of herbal medicines in lung cancer treatment.

摘要

随着关于草药治疗效果和安全性的证据不断增加,其在肺癌治疗中的应用大幅增加。与此同时,它们在系统层面的作用机制尚未得到全面揭示。为此,我们采用网络药理学方法来阐明FDY2004(一种由牡丹皮、桃仁和大黄组成的抗癌草药)在肺癌治疗中的系统作用机制。通过使用与草药相关的数据库评估FDY2004中存在的化合物的药代动力学特性,我们确定了其29种活性化学成分与141个与人类肺癌相关的治疗靶点相互作用。对FDY2004的肺癌相关靶点进行功能富集分析,揭示了富集的基因本体学术语,涉及细胞增殖和生长的调节、细胞存活和死亡以及氧化应激反应。此外,我们确定了与肺癌相关的关键FDY2004靶向致癌和肿瘤抑制途径,包括磷脂酰肌醇3-激酶-蛋白激酶B、丝裂原活化蛋白激酶、肿瘤坏死因子、Ras、粘着斑和缺氧诱导因子-1信号通路。总体而言,我们的研究为草药在肺癌治疗中的综合抗癌机制研究提供了新的证据和依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/94a3438d0ed1/ECAM2021-6644018.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/046eaf769b53/ECAM2021-6644018.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/fe277428b029/ECAM2021-6644018.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/878303ec0005/ECAM2021-6644018.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/51a454ef366d/ECAM2021-6644018.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/94a3438d0ed1/ECAM2021-6644018.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/046eaf769b53/ECAM2021-6644018.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/fe277428b029/ECAM2021-6644018.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/878303ec0005/ECAM2021-6644018.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/51a454ef366d/ECAM2021-6644018.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a2a/7886515/94a3438d0ed1/ECAM2021-6644018.005.jpg

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