Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology

Rui TAO; Guan-wei FAN; Hao-ping MAO; Xiao-ying WANG; Lin MIAO; Xiu-mei GAO

doi:10.13422/j.cnki.syfjx.20190508

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Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology

Data Mining | 更新时间：2021-02-09

- Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 5, Pages: 208-213(2019)
- 作者机构：
  
  1.天津中医药大学　中医药研究院，天津市现代中药重点实验室，天津市中药药理学重点实验室，天津　 300193；
  2.天津中医药大学　第一附属医院，天津　 300193
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20190508
  CLC： R2-0;R22;R285.5;R289
- Received：31 August 2018，
  
  Published Online：21 November 2018，
  
  Published：05 March 2019
- 稿件说明：
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Rui TAO, Guan-wei FAN, Hao-ping MAO, et al. Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(5): 208-213.
DOI：

Rui TAO, Guan-wei FAN, Hao-ping MAO, et al. Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(5): 208-213. DOI： 10.13422/j.cnki.syfjx.20190508.

摘要

目的：

基于网络药理学预测二至丸治疗良性前列腺增生的作用靶点，探讨其多成分-多靶点-多通路的作用机制，对其治疗良性前列腺增生的分子机制进行科学阐释。

方法：

采用网络药理学软件生物反应路径分析(IPA)构建“化合物-靶点-疾病”的网络；对二至丸作用靶点构建蛋白互作网络(PPI)，进行基因富集分析(GO)功能注释和京都基因和基因组百科全书(KEGG)通路富集分析，预测二至丸治疗前列腺增生的作用机制。

结果：

二至丸总共有19个化合物在IPA中，并且芹菜素(Apigenin)，木犀草素(Luteolin)，熊果酸(Oleanolic acid)和槲皮苷(Quercitrin)4个化合物是女贞子和墨旱莲共有化合物，是二至丸的主要物质基础；毒蕈碱型乙酰胆碱受体M3(CHRM3)，毒蕈碱型乙酰胆碱受体M2(CHRM2)，尿激酶型纤溶酶原激活物受体(PLAUR)，激肽释放酶3(KLK3)，钙黏蛋白1(CDH1)，趋化因子3(CCL3)和金属蛋白酶1(MMP1)等二至丸治疗前列腺增生的关键靶点；PPI网络靶点蛋白有20条GO功能富集和5条主要的KEGG通路富集，并对相关靶点进行Docking验证。

结论：

二至丸通过激活MMP1和抑制KLK3以及CCL3蛋白表达，诱导细胞凋亡和抑制细胞增殖，干预丝裂原活化蛋白激酶／胞外信号调节激酶(MAPK/ERK)，核转录因子-

B(NF-

B)等信号通路发挥抑制前列腺增生的作用。

Abstract

Objective:

To explain the "multi-components

multi-targets

multi-pathways" mechanism of Erzhiwan in treating benign prostatic hyperplasia(BPH) based the network pharmacology.

Method:

Ingenuity pathway analysis(IPA) was used to construct components-targets-diseases network and PPI network

then the classified enrichment analysis of gene ontology (GO) and pathway enrichment analysis (KEGG) were carried out on the main function of its gene sets

so as to discuss the mechanism of Erzhiwan in the treatment of BPH.

Result:

Erzhiwan has 19 components in IPA; and apigenin

luteolin

oleanolic acid and quercitrin were common components of Ligustri Lucidi Fructus and Echiptae Herba and the main component of Erzhiwan. Muscarinic acetylcholine receptor M3 (CHRM3)

muscarinic acetylcholine receptor M2 (CHRM2)

urokinase plasminogen activator receptor (PLAUR)

kinin releasing enzyme 3 (KLK3)

cadherin 1 (CDH1)

chemokines 3 (CCL3) and metalloproteinase-1 (MMP-1) were important targets for Erzhiwan to treat BPH. The target proteins in PPI network were enriched with 20 GO functions and 5 main KEGG pathways

and Docking was verified for relevant targets.

Conclusion:

Erzhiwan may play a role in treating BPH by activating MMP-1 and inhibiting KLK3 and CCL3 protein expressions

inducing apoptosis

inhibiting cell proliferation and intervening relevant pathways of mitogen-activated protein kinase/extracellular signal-regulated kinase(MAPK/ERK) and nuclear factor(NF)-

B(NF-

B).

关键词

Keywords

references

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