Mechanism of <italic style="font-style: italic">Eucommia</italic> <italic style="font-style: italic">ulmoides</italic> against osteoporosis based on network pharmacology, molecular docking, and experimental verification

LIU Ping; QI Baoyu; WEI Xu; ZHU Liguo; SUN Kai; ZHANG Yili; LU Jiajin

doi:10.16025/j.1674-1307.2026.02.008

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Mechanism of Eucommia ulmoides against osteoporosis based on network pharmacology, molecular docking, and experimental verification

更新时间：2026-04-08

- Mechanism of Eucommia ulmoides against osteoporosis based on network pharmacology, molecular docking, and experimental verification
- Beijing Journal of Traditional Chinese Medicine Vol. 45, Issue 2, Pages: 196-203(2026)
- 作者机构：
  
  1.北京中医药大学中医学院，北京 100029
  2.中国中医科学院望京医院脊柱二科，北京100102
  3.数智中医防治骨与关节退行性疾病北京市重点实验室，北京 100102
  4.南京中医药大学中西医结合学院，南京 210023
- 作者简介：
- 基金信息：
- DOI：10.16025/j.1674-1307.2026.02.008
  CLC：
- Received：23 March 2025，
  
  Published：25 February 2026
- 稿件说明：
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刘平，齐保玉，魏戌，等.基于网络药理学、分子对接及实验验证探究杜仲抗骨质疏松症的作用机制［J］.北京中医药，2026，45（2）：196-203.

LIU Ping,QI Baoyu,WEI Xu,et al.Mechanism of Eucommia ulmoides against osteoporosis based on network pharmacology, molecular docking, and experimental verification[J]. Beijing Journal of Traditional Chinese Medicine,2026,45(02):196-203.
刘平，齐保玉，魏戌，等.基于网络药理学、分子对接及实验验证探究杜仲抗骨质疏松症的作用机制［J］.北京中医药，2026，45（2）：196-203. DOI： 10.16025/j.1674-1307.2026.02.008.

LIU Ping,QI Baoyu,WEI Xu,et al.Mechanism of Eucommia ulmoides against osteoporosis based on network pharmacology, molecular docking, and experimental verification[J]. Beijing Journal of Traditional Chinese Medicine,2026,45(02):196-203. DOI： 10.16025/j.1674-1307.2026.02.008.

摘要

目的

通过网络药理学、分子对接联合体外细胞实验探究杜仲治疗骨质疏松症的核心靶点及作用机制。

方法

利用中药系统药理学数据库（TCMSP）获取杜仲活性成分及作用靶点，使用GeneCards、DisGeNET、OMIM数据库获取骨质疏松症的疾病靶点，构建蛋白-蛋白互作网络及“活性成分-共同靶点”网络。通过Metascape数据库对关键靶点进行生物功能和信号通路分析，使用AutoDock软件对核心成分和关键靶点进行分子对接及结果可视化。构建体外成骨细胞模型，用细胞计数试剂盒-8、茜素红染色等方法检测细胞增殖和矿化能力，免疫印记（WB）法检测胶原蛋白Ⅰ（Col-Ⅰ）、Runt相关转录因子2（Runx2）、蛋白激酶B1（AKT1）AKT1蛋白表达。

结果

获得28个杜仲有效活性成分、221个作用靶点、2 661个骨质疏松症疾病靶点；通过靶点映射筛选出杜仲抗骨质疏松症的潜在靶点80个，核心靶点为AKT1、肿瘤坏死因子（TNF）、缺氧诱导因子1α（HIF1A）等。富集分析后获得与骨质疏松症密切相关的信号通路6条。分子对接结果显示，杜仲中山柰酚、槲皮素可与AKT1、HIF1A和TNF蛋白结合。体外细胞实验表明，杜仲活性成分山柰酚可增加细胞活力，升高AKT1、Col-Ⅰ、Runx2蛋白表达水平。

结论

杜仲可能通过调控AKT1表达，促进成骨细胞增殖、分化和矿化，从而发挥治疗骨质疏松症的作用。

Abstract

Objective

To explore the core targets and mechanisms of

Eucommia ulmoides

in the treatment of osteoporosis through network pharmacology， molecular docking， and in vitro cell experiments.

Methods

Active components and targets of

E. ulmoides

were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， and osteoporosis-related disease targets were retrieved from GeneCards， DisGeNET， and OMIM databases. Protein-protein interaction network and "active component-common target" network were constructed. Key targets were analyz

ed for biological functions and signaling pathways using the Metascape database. Molecular docking between core components and key targets was performed and visualized using AutoDock software. An in vitro osteoblast model was established， and cell proliferation and mineralization were assessed by CCK-8 assay and Alizarin Red staining. Western blot was used to detect the protein expression of collagen I （Col-I）， runt-related transcription factor 2 （Runx2）， and protein kinase B1 （AKT1）.

Results

A total of 28 active components of

E. ulmoides

， 221 targets， and 2 661 osteoporosis-related disease targets were identified. Target mapping screened 80 potential targets for osteoporosis， with core targets including AKT1， tumor necrosis factor （TNF）， and hypoxia-inducible factor 1α （HIF1A）. Enrichment analysis identified six signaling pathways closely related to osteoporosis. Molecular docking showed that chlorogenic acid and quercetin from

E. ulmoides

can bind to AKT1， HIF1A， and TNF proteins. In vitro experiments demonstrated that chlorogenic acid， an active component of

E. ulmoides

， increased cell viability and upregulated the protein expression of AKT1， Col-I， and Runx2.

Conclusion

E. ulmoides

may exert therapeutic effects in osteoporosis by regulating AKT1 expression and promoting osteoblast proliferation， differentiation， and mineralization.

关键词

Keywords

references

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Mechanism of Eucommia ulmoides against osteoporosis based on network pharmacology, molecular docking, and experimental verification

DOI：10.16025/j.1674-1307.2026.02.008

摘要

Abstract

关键词

Keywords

references