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Network Pharmacology-Based Investigation on the Anti-Osteoporosis Mechanism of Astragaloside IV
Natural Product Communications ( IF 1.8 ) Pub Date : 2021-07-08 , DOI: 10.1177/1934578x211029549
Li Ou 1 , Wenqian Kang 1 , Jiahao Zhang 1 , Peifeng Wei 1 , Min Li 1 , Feng Gao 1 , Taiwei Dong 1
Affiliation  

Astragaloside IV is the main active ingredient of Astragalus membranaceus. Studies have found that it can promote the proliferation of osteoblasts and can antagonize the apoptosis of mouse osteoblasts induced by hydrogen peroxide, but its molecular mechanism for the treatment of osteoporosis is still not clear. First, we used 3 online platforms: CTD, PharmMapper and SwissTargetPrediction to retrieve the targets of Astragaloside IV, and collected osteoporosis-related targets. Next, we used Cytoscape 3.7.2 software to construct a visual network diagram of PPI and further screened the key genes of Astragaloside IV in the treatment of osteoporosis using cluster analysis. Finally, after the receptor and ligand were docked, the binding activity was assessed by docking score. We obtained 102 overlapping targets of Astragaloside IV and osteoporosis. According to the node degree value in the PPI network, the top 10 genes were PIK3CA, MAPK1, SRC, STAT3, VEGFA, HSP90AA1, RELA, AKT1, IGF1, EGFR, of which SRC, AKT1, PIK3CA could bind stably to Astragaloside IV. KEGG pathway enrichment results showed that Astragaloside IV treated osteoporosis through 10 main pathways, including PI3K-Akt signaling pathway, FoxO signaling pathway, MAPK pathway, and so on. The classification of these pathways belongs to signal transduction, immune system, development and regeneration and endocrine system. Astragaloside IV is significantly related to several pathways involved in osteoporosis, such as PI3K-Akt, FoxO signaling pathway and MAPK pathway. SRC, AKT1, and PIK3CA can bind stably with Astragaloside IV, and they may be hub genes for the treatment of osteoporosis.



中文翻译:

基于网络药理学的黄芪甲苷抗骨质疏松机制研究

黄芪是主要活性成分黄芪. 研究发现它可以促进成骨细胞的增殖,可以拮抗过氧化氢诱导的小鼠成骨细胞的凋亡,但其治疗骨质疏松症的分子机制尚不清楚。首先,我们使用CTD、PharmMapper和SwissTargetPrediction 3个在线平台检索黄芪甲苷的靶点,收集骨质疏松相关的靶点。接下来,我们使用Cytoscape 3.7.2软件构建了PPI的可视化网络图,并通过聚类分析进一步筛选了黄芪甲苷治疗骨质疏松症的关键基因。最后,受体和配体对接后,通过对接评分评估结合活性。我们获得了 102 个与黄芪甲苷和骨质疏松症重叠的靶点。根据PPI网络中的节点度值,前10位基因为PIK3CA、MAPK1、SRC、STAT3、VEGFA、HSP90AA1、RELA、AKT1、IGF1、EGFR,其中SRC、AKT1、PIK3CA与黄芪甲苷能稳定结合。KEGG通路富集结果显示黄芪甲苷通过PI3K-Akt信号通路、FoxO信号通路、MAPK通路等10条主要通路治疗骨质疏松症。这些通路的分类属于信号转导、免疫系统、发育再生和内分泌系统。黄芪甲苷与参与骨质疏松症的几种通路显着相关,如 PI3K-Akt、FoxO 信号通路和 MAPK 通路。SRC、AKT1和PIK3CA可以与黄芪甲苷稳定结合,可能是治疗骨质疏松症的枢纽基因。PIK3CA 可以与黄芪甲苷稳定结合。KEGG通路富集结果显示黄芪甲苷通过PI3K-Akt信号通路、FoxO信号通路、MAPK通路等10条主要通路治疗骨质疏松症。这些通路的分类属于信号转导、免疫系统、发育再生和内分泌系统。黄芪甲苷与参与骨质疏松症的几种通路显着相关,如 PI3K-Akt、FoxO 信号通路和 MAPK 通路。SRC、AKT1和PIK3CA可以与黄芪甲苷稳定结合,可能是治疗骨质疏松症的枢纽基因。PIK3CA 可以与黄芪甲苷稳定结合。KEGG通路富集结果显示黄芪甲苷通过PI3K-Akt信号通路、FoxO信号通路、MAPK通路等10条主要通路治疗骨质疏松症。这些通路的分类属于信号转导、免疫系统、发育再生和内分泌系统。黄芪甲苷与参与骨质疏松症的几种通路显着相关,如 PI3K-Akt、FoxO 信号通路和 MAPK 通路。SRC、AKT1和PIK3CA可以与黄芪甲苷稳定结合,可能是治疗骨质疏松症的枢纽基因。等等。这些通路的分类属于信号转导、免疫系统、发育再生和内分泌系统。黄芪甲苷与参与骨质疏松症的几种通路显着相关,如 PI3K-Akt、FoxO 信号通路和 MAPK 通路。SRC、AKT1和PIK3CA可以与黄芪甲苷稳定结合,可能是治疗骨质疏松症的枢纽基因。等等。这些通路的分类属于信号转导、免疫系统、发育再生和内分泌系统。黄芪甲苷与参与骨质疏松症的几种通路显着相关,如 PI3K-Akt、FoxO 信号通路和 MAPK 通路。SRC、AKT1和PIK3CA可以与黄芪甲苷稳定结合,可能是治疗骨质疏松症的枢纽基因。

更新日期:2021-07-08
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