| 基于网络药理学的青蒿治疗肾阴虚型糖皮质激素性骨质疏松机制研究 |
| 投稿时间：2022-04-27 修订日期：2022-11-01 点此下载全文 |
| 引用本文：赖立勇,夏天爽,岳小强,辛海量.基于网络药理学的青蒿治疗肾阴虚型糖皮质激素性骨质疏松机制研究[J].药学实践杂志,2023,41(11):672~679 |
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| 中文摘要:目的 通过网络药理学和体外实验，对青蒿治疗肾阴虚型糖皮质激素性骨质疏松（GIOP）的潜在作用靶点及相关信号通路进行预测和初步验证。方法 通过TCMSP数据库和Uniprot数据库获取青蒿药物靶点并确定目标靶点基因名；通过GeneCards数据库、OMIM数据库和Drugbank数据库获取肾阴虚型GIOP的靶点基因，与药物靶点基因交叉分析获得共同作用靶点基因；利用String数据库构建蛋白质-蛋白质相互作用（PPI）网络，并利用Cytoscape软件进行可视化分析和核心靶点筛选；通过Metascape数据库对所有共同靶点进行基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析，最后通过体外实验对预测结果进行验证。结果 筛选出98个青蒿治疗肾阴虚型GIOP的作用靶点，其中核心基因17个。GO和KEGG功能富集分析结果表明，青蒿治疗肾阴虚型GIOP与激素应答、细胞死亡的正向调节和细胞外刺激应答等生物过程，以及PI3K/AKT、AGE/RAGE、MAPK和IL-17等信号通路有关，其中PI3K/AKT信号通路上富集的基因数最多。体外实验结果显示，青蒿可以促进地塞米松（DEX）损伤的成骨细胞的增殖，提高碱性磷酸酶（ALP）活性，激活PI3K/AKT通路，促进AKT的磷酸化。结论 青蒿治疗肾阴虚型GIOP具有多靶点‐多通路的特点，可以通过多条途径促进成骨细胞的增殖、分化，其中PI3K/AKT信号通路是一条重要的通路，青蒿治疗肾阴虚型GIOP可能与其能够促进PI3K/AKT信号通路，促进AKT的磷酸化有关。 |
| 中文关键词:青蒿 肾阴虚 糖皮质激素性骨质疏松 地塞米松 成骨细胞 |
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| Mechanism of Artemisia annua L. in GIOP with kidney-yin deficiency based on network pharmacology |
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| Abstract:Objective To predict and preliminarily verify the potential targets and related signaling pathways of Artemisia annua L. in treating glucocorticoid-induced osteoporosis (GIOP) with kidney-yin deficiency by network pharmacology and in vitro experiments. Methods The pharmacological targets of Artemisia annua L. were obtained from TCMSP database and were converted to gene names through Uniprot database. The target genes of GIOP with kidney-yin deficiency were obtained from GeneCards database, OMIM database and Drugbank database, and the common target genes were obtained by cross analysis with drug target gene. Protein-protein interaction (PPI) network was constructed by String database, and visualization analysis and core targets screening were performed by Cytoscape 3.9.0. All common targets were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis through Metascape database. Finally, the prediction results were verified by in vitro experiments. Results Ninety-eight targets of Artemisia annua L. to GIOP with kidney-yin deficiency were screened, including 17 core genes. The results of GO and KEGG functional enrichment analysis indicated that Artemisia annua L. treating GIOP with kidney-yin deficiency was related to biological processes such as hormonal response, positive regulation of cell death and extracellular stimulation response, et al, as well as signaling pathways such as PI3K/AKT, AGE/RAGE, MAPK and IL-17 et al. The number of genes enriched in PI3K/AKT signaling pathway was the largest. In vitro experiment results showed that Artemisia annua L. promoted the proliferation of osteoblasts damaged by dexamethasone (DEX), increased alkaline phosphatase activity, activated PI3K/AKT pathway, and promoted the phosphorylation of AKT. Conclusion Artemisia annua L. treating GIOP with kidney-yin deficiency has the characteristics of multi-targets and multi-pathway, which could promote the proliferation and differentiation of osteoblasts through multiple pathways. The PI3K/AKT signaling pathway is an important pathway. Artemisia annua L. treating GIOP with kidney-yin deficiency might be related to its ability to promote the PI3K/AKT signaling pathway and promote the phosphorylation of AKT. |
| keywords:Artemisia annua L. kidney-yin deficiency glucocorticoid-induced osteoporosis dexamethasone osteoblast |
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