Network pharmacology explores the mechanisms of Eucommia ulmoides cortex against postmenopausal osteoporosis

被引:8
|
作者
Shao, Yan [1 ]
Chen, Song [2 ]
Zhou, Ke [3 ]
Gan, Kaifeng [3 ]
Li, Jin [3 ]
Xia, Chenjie [3 ]
机构
[1] Zhejiang Univ, Shengzhou Branch, Affiliated Hosp 1, Dept Pharm,Shengzhou Peoples Hosp, Shengzhou, Peoples R China
[2] Third Peoples Med & Hlth Grp Cixi City, Dept Orthoped Surg, Ningbo, Peoples R China
[3] Ningbo Univ, Li Huili Hosp, Dept Orthoped Surg, Ningbo, Peoples R China
基金
中国国家自然科学基金;
关键词
database; Eucommia ulmoides; herb medicine; network pharmacology; postmenopausal osteoporosis; NF-KAPPA-B; SIGNALING PATHWAY; ANGIOGENESIS; OSTEOGENESIS;
D O I
10.1097/MD.0000000000029257
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Postmenopausal osteoporosis (PMOP) has become one of most frequent chronic disease worldwide with aging population. Eucommia ulmoides cortex (EU), a traditional Chinese medicine, has long since been used to treat PMOP. The aim of this study is to explore pharmacological mechanisms of EU against PMOP through using network pharmacology approach. The active ingredients of EU were obtained from Traditional Chinese Medicine System Pharmacology database, and target fishing was performed on these ingredients in UniProt database for identification of their relative targets. Then, we screened the targets of PMOP using GeneCards database and DisGeNET database. The overlapping genes between PMOP and EU were obtained to performed protein-protein interaction, Gene Ontology analysis, Kyoto encyclopedia of genes, and genomes analysis. Twenty-eight active ingredients were identified in EU, and corresponded to 207 targets. Also, 292 targets were closely associated with PMOP, and 50 of them matched with the targets of EU were considered as therapeutically relevant. Gene ontology enrichment analysis suggested that EU exerted anti-PMOP effects via modulating multiple biological processes including cell proliferation, angiogenesis, and inflammatory response. Kyoto encyclopedia of genes and genomes enrichment analysis revealed several pathways, such as PI3K-AKT pathway, mitogen-activated protein kinase pathway, hypoxia-inducible factors-1 pathway, tumor necrosis factor pathway, and interleukin-17 pathway that might be involved in regulating the above biological processes. Through the method of network pharmacology, we systematically investigated the mechanisms of EU against PMOP. The multi-targets and multi-pathways identified here could provide new insights for further determination of more exact mechanisms of EU.
引用
收藏
页数:8
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