Potential Mechanism of Panax notoginseng for Coronary Heart Disease Based on the Network Pharmacology
- VernacularTitle:基于网络药理学探究三七治疗冠心病的潜在作用机制
- Author:
Guifeng HUANG
1
;
Xiaohong ZHENG
1
;
Zhexing MAI
2
;
Zhaojun YANG
2
;
Xueying LIN
3
;
Junzhe LI
2
Author Information
1. Dept. of Cardiovascular Medicine，Shantou Chaoyang District Dafeng Hospital，Guangdong Shantou 515100，China
2. Second College of Clinical Medicine，Guangzhou University of TCM，Guangzhou 510405，China
3. First College of Clinical Medicine，Guangzhou University of TCM，Guangzhou 510405，China
- Publication Type:Journal Article
- Keywords:
Panax notoginseng;
Coronary heart disease;
Network pharmacology;
Component;
Target;
Pathway;
Mechanism
- From:
China Pharmacy
2019;30(14):1959-1965
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE： To explore the component， target and pathway of Panax notoginseng for coronary heart disease （CHD） and its potential molecular mechanism. METHODS： Based on network pharmacology， active components of P. notoginseng were retrieved with TCMSP platform. The targets of P. notoginseng for CHD were screened by using DRAR-CPI server， GeneCards and DisGeNET databases. Cytoscape 3.6.0 software was used to form the effective components-CHD targets network of P. notoginseng. String database was used to draw target interaction network. Network Analyzer tool was used to calculate target connectivity， and potential core targets were screened. Molecular docking between the core targets and the effective components of P. notoginseng was performed by Systems Dock Web Site server. KEGG pathway enrichment analysis and gene ontology （GO） enrichment analysis were also carried out to explore the important signal pathway and molecular function of P. notoginseng for CHD. “Effective component-target-signal pathway”network of important signal pathway were constructed. RESULTS： Five effective components （stigmasterol， β-sitosterol， ginsenoside rh2， quercetin， notoginsenoside r1） were screened from P. notoginseng for CHD， which acted on 96 targets and had 134 functional relationships. Five core targets were protein kinase B （AKT）， interleukin 6 （IL-6）， vascular endothelial growth factor A （VEGFA）， c-JUN protein （c-JUN） and heparin binding epidermal growth factor （HB-EGF）， which played an important role in the treatment of CHD by altering protein binding and regulating signaling pathways as phosphatidylinositol-3 kinase-protein/kinase B （PI3K/AKT）， hypoxia-inducible factor-1 （HIF-1） and mitogen-activated protein kinase （MAPK）. CONCLUSIONS： P. notoginseng in the treatment of CHD is not only play a variety of effects through the role of multiple targets， but also produce complex network regulation effect through the interaction between targets.
