Molecular Mechanism of Erzhiwan in Inhibiting Benign Prostatic Hyperplasia Base on Network Pharmacology
10.13422/j.cnki.syfjx.20190508
- VernacularTitle: 基于网络药理学探究二至丸抑制良性前列腺增生的分子机制
- Author:
Rui TAO
1
;
Guan-wei FAN
1
;
Hao-ping MAO
1
;
Xiao-ying WANG
1
;
Lin MIAO
1
;
Xiu-mei GAO
1
Author Information
1. Tianjin University of Traditional Chinese Medicine(TCM), Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin Key Laboratory of TCM Pharmacology, Tianjin 300193, China
- Publication Type:Research Article
- Keywords:
network pharmacology;
Erzhiwan;
Ligustri Lucidi Fructus;
Echiptae Herba;
benign prostatic hyperplasia
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(5):208-213
- CountryChina
- Language:Chinese
-
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)-κB(NF-κB).
