基于HPLC-Q-Exactive-MS/MS整合网络药理学研究加味塔布森-2有效成分及其抗骨质疏松机制

Study on the Effective Ingredients of Modified Tubson-2 and Its Anti-osteoporosis Mechanism Based on HPLC-Q-Exactive-MS/MS Integrated Network Pharmacology

关键词:  HPLC-Q-Exactive-MS/MS  加味塔布森-2  入血成分  网络药理  骨质疏松  分子对接

Key words:  HPLC-Q-Exactive-MS/MS  Modified Tubson-2  blood components  network pharmacology  osteoporosis  molecular docking

摘要:

目的 鉴定加味塔布森-2入血成分，并结合网络药理学阐述其治疗骨质疏松的作用机制。方法 采用HPLC-Q-Exactive-MS/MS对加味塔布森-2入血成分进行鉴定；在此基础上结合SwissTarget Prediction与SuperPred数据库进行入血成分的靶点预测，同时在DisGeNET数据库中搜索骨质疏松相关的疾病靶点，利用Cytoscape软件构建"入血成分-靶点-疾病"网络模型，运用String数据分析平台进行蛋白互作网络分析，并且利用David数据库对核心靶点进行GO富集分析和KEGG通路分析，最后使用分子对接对网络药理学内容进行初步验证。结果 最终确定入血成分21个，通过网络药理分析得到加味塔布森-2抗骨质疏松的核心靶点11个。对11个核心靶点进行GO功能注释和KEGG通路分析后，发现加味塔布森-2抗骨质疏松的信号通路主要包括HIF-1、雌激素、MAPK、甲状腺素、TNF、mTOR、PI3K/AKT等。结论 该方法初步明确了加味塔布森-2的入血成分及潜在作用机制，为加味塔布森-2药理作用机制的进一步研究提供科学依据。

Abstract:

OBJECTIVE To identify the blood components of Modified Tubson-2, and to elucidate its mechanism of treatment of osteoporosis combine with network pharmacology. METHODS HPLC-Q-Exactive-MS/MS was used to identify the blood components of Modified Tubson-2; on this basis, the target prediction of blood components was conducted with SwissTarget Prediction and SuperPred database. At the same time, DisGeNET database was used to search for disease targets related to osteoporosis. Cytoscape software was employed to build a "blood component-target-disease" network model. Then String database platform was used to perform protein interaction network analysis. And David database was used for GO enrichment analysis and KEGG pathway analysis of core targets. Finally, the results of network pharmacology were validated by using Autoduck software. RESULTS Finally, 21 blood components were determined. Eleven core targets of Modified Tubson-2 anti-osteoporosis were obtained through network pharmacological analysis. According to the results of GO function annotation and KEGG pathway analysis of 11 core targets, Modified Tubson-2 treating osteoporosis mainly involved in the HIF-1, estrogen, MAPK, thyroxine, TNF, mTOR, PI3K/AKT signaling pathways. CONCLUSION This method preliminarily clarifies the blood components and potential mechanism of the Modified Tubson-2, and provides an important reference for further research on the pharmacological mechanisms of Modified Tubson-2.