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皂苷预防深静脉血栓形成的网络药理学分析与临床验证

Network pharmacology analysis and clinical verification of saponins in deep venous thrombosis prevention.

作者信息

Yan Bin, Ning Yachan, Guo Julong, Liu Limin, Wang Chunmei

机构信息

Department of Intensive Care Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.

Department of Vascular Surgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.

出版信息

Biomed Rep. 2024 Nov 1;22(1):8. doi: 10.3892/br.2024.1886. eCollection 2025 Jan.

DOI:10.3892/br.2024.1886
PMID:39559819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11572032/
Abstract

In the present study, the mechanism of saponins (PNS), the extract of , against deep vein thrombosis (DVT) was explored by networks pharmacology and its effect was demonstrated through clinical data. PNS includes 5 main active components, which have 101 targets. A total of 1,342 DVT-related targets were obtained, 55 of which were the common targets of PNS and DVT. AKT1, TNF, IL1B, EGFR, VEGFA and MAPK3 were selected as hub genes from the protein-protein interaction network. The potential anti-DVT mechanism of PNS may involve the AGE-RAGE signaling pathway and the PI3K-Akt signaling pathway. Molecular docking presented a total of 10 binding interactions, with all molecules showing good binding ability with PNS-DVT common hub target genes (all binding energy <-6 kcal/mol). Analysis of clinical data showed that the combined use of PNS significantly reduced the incidence of postoperative DVT in patients undergoing orthopedic surgery compared with the use of low-molecular-weight heparin alone, which is the most commonly used clinical anticoagulant.

摘要

在本研究中,通过网络药理学探索了三七总皂苷(PNS)提取物抗深静脉血栓形成(DVT)的机制,并通过临床数据证实了其效果。PNS包括5种主要活性成分,共有101个靶点。共获得1342个DVT相关靶点,其中55个是PNS和DVT的共同靶点。从蛋白质-蛋白质相互作用网络中选择AKT1、TNF、IL1B、EGFR、VEGFA和MAPK3作为枢纽基因。PNS潜在的抗DVT机制可能涉及晚期糖基化终产物受体(AGE-RAGE)信号通路和磷脂酰肌醇-3激酶-蛋白激酶B(PI3K-Akt)信号通路。分子对接共呈现10种结合相互作用,所有分子与PNS-DVT共同枢纽靶基因均显示出良好的结合能力(所有结合能<-6千卡/摩尔)。临床数据分析表明,与单独使用临床最常用的抗凝剂低分子量肝素相比,联合使用PNS可显著降低骨科手术患者术后DVT的发生率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/b33fe89234b4/br-22-01-01886-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/75a36cbbe490/br-22-01-01886-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/0ca10da207da/br-22-01-01886-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/16877bf391ea/br-22-01-01886-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/498d83688277/br-22-01-01886-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/b33fe89234b4/br-22-01-01886-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/75a36cbbe490/br-22-01-01886-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/0ca10da207da/br-22-01-01886-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/16877bf391ea/br-22-01-01886-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/498d83688277/br-22-01-01886-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596a/11572032/b33fe89234b4/br-22-01-01886-g04.jpg

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本文引用的文献

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Astragaloside IV induces endothelial progenitor cell angiogenesis in deep venous thrombosis through inactivation of PI3K/AKT signaling.黄芪甲苷通过抑制 PI3K/AKT 信号通路诱导深静脉血栓形成中的血管生成。
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The Role of EGFR Amplification in Deep Venous Thrombosis Occurrence in IDH Wild-Type Glioblastoma.
表皮生长因子受体(EGFR)扩增在异柠檬酸脱氢酶(IDH)野生型胶质母细胞瘤深静脉血栓形成中的作用
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Dematin Regulates Calcium Mobilization, Thrombosis, and Early Akt Activation in Platelets.德马丁调节血小板中的钙动员、血栓形成和早期 Akt 激活。
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