[基于网络药理学探讨复方钩藤降压片治疗高血压的作用机制]。

PubMed ID
G H
发表日期 2018年Apr月

原始出处 中国中药杂志
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
作者 Long  Hong-Ping  Lin  Xiao-Yuan  Wang  Yu-Hong  Ren  Wei-Qiong  Shao  Le  Zhang  Wen  Tan  Yuan-Sheng 

文献标题 [基于网络药理学探讨复方钩藤降压片治疗高血压的作用机制]。
[Explore mechanism of Compound Uncaria Hypotensive Tablet for hypertension based on network pharmacology].
[Explore mechanism of Compound Uncaria Hypotensive Tablet for hypertension based on network pharmacology].

文献摘要

以网络药理学为基础,预测复方钩藤降压片的有效成分和作用靶点,探讨其治疗高血压可能的“多成分、多靶点、多途径”机制。利用中药综合药理平台(TCM-IP)构建复方钩藤降压片组分靶向疾病靶向网络,采用互联网分析方法筛选关键节点,在此基础上进行路径富集分析,探讨其治疗高血压的可能生物学过程。靶网络分析表明,35种预测的复方钩藤降压片有效成分与前列腺素内源性过氧化物酶合酶(PTGS1、PTGS2)、ATP合成酶(ATP1A1、ATP5A1、ATP5C1、ATP5B)等29种主要蛋白有较强的相互作用。网络富集分析表明,复方钩藤降压片通过调节血压、G蛋白偶联受体激活、肾上腺素能心肌细胞信号转导和血小板活化等15条途径参与了高血压不同病理过程的调节。本研究揭示了复方钩藤降压片治疗高血压的潜在活性成分及可能的作用机制,为进一步开展复方钩藤降压片有效成分及作用机制的系统实验提供了理论参考。


This paper aimed to predict the active ingredients and action targets of Compound Uncaria Hypotensive Tablet for hypertension based on network pharmacology, and discuss its possible "multi-components, multi-targets, and multi-pathways" mechanism for treatment of hypertension. The integrative pharmacological platform of traditional Chinese medicine (TCM-IP) was used to construct the component target-disease target network of Compound Uncaria Hypotensive Tablet, and the internet analysis method was used to screen the key nodes, on which the pathway enrichment analysis was carried out to explore its possible biological process in the treatment of hypertension. Target network analysis showed that, 35 predicted active ingredients of Compound Uncaria Hypotensive Tablet had a strong interaction with the prostaglandin endogenous peroxidase synthase (PTGS1, PTGS2), ATP synthetase (ATP1A1, ATP5A1, ATP5C1, ATP5B) and other 29 major proteins. Network enriched analysis showed that Compound Uncaria Hypotensive Tablet participated in the regulation of hypertension in different processes of pathology, through 15 pathways such as regulating blood pressure, G protein coupled receptor activation, adrenergic myocardial cell signal transduction and platelet activation. This study revealed the potential active compounds and possible mechanism of Compound Uncaria Hypotensive Tablet for treatment of hypertension, providing theoretical references for further systematic laboratory experiments on effective compounds and action mechanism of Compound Uncaria Hypotensive Tablet.

This paper aimed to predict the active ingredients and action targets of Compound Uncaria Hypotensive Tablet for hypertension based on network pharmacology, and discuss its possible "multi-components, multi-targets, and multi-pathways" mechanism for treatment of hypertension. The integrative pharmacological platform of traditional Chinese medicine (TCM-IP) was used to construct the component target-disease target network of Compound Uncaria Hypotensive Tablet, and the internet analysis method was used to screen the key nodes, on which the pathway enrichment analysis was carried out to explore its possible biological process in the treatment of hypertension. Target network analysis showed that, 35 predicted active ingredients of Compound Uncaria Hypotensive Tablet had a strong interaction with the prostaglandin endogenous peroxidase synthase (PTGS1, PTGS2), ATP synthetase (ATP1A1, ATP5A1, ATP5C1, ATP5B) and other 29 major proteins. Network enriched analysis showed that Compound Uncaria Hypotensive Tablet participated in the regulation of hypertension in different processes of pathology, through 15 pathways such as regulating blood pressure, G protein coupled receptor activation, adrenergic myocardial cell signal transduction and platelet activation. This study revealed the potential active compounds and possible mechanism of Compound Uncaria Hypotensive Tablet for treatment of hypertension, providing theoretical references for further systematic laboratory experiments on effective compounds and action mechanism of Compound Uncaria Hypotensive Tablet.


获取全文 10.19540/j.cnki.cjcmm.20180115.010