清热活血方抑制类风湿关节炎血管生成的机制:基于网络药理学和体外实验。

IF 2 4区 医学 Q3 PHYSIOLOGY Journal of Physiology and Pharmacology Pub Date : 2023-02-01 DOI:10.26402/jpp.2023.1.06
X Zhang, K Zhi, Y Yang, W Cui, L Cai, X Zhao, Z Zhang, W Cao
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引用次数: 0

摘要

本研究旨在基于网络药理学和体外实验,探讨清热活血方(QRHXF)抗类风湿性关节炎(RA)血管生成的作用机制。我们利用中药系统药理学数据库和分析平台(TCMSP)和治疗靶点(TTD)数据库提取QRHXF的有效成分和调节血管生成的潜在靶点。首先,我们利用Cytoscape生物信息学软件构建qrhxf血管生成网络,筛选潜在靶点。然后,我们对潜在核心靶点进行了基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析。此外,采用酶联免疫法和Western blot法进行体外验证,验证不同浓度QRHXF对人脐静脉内皮细胞(HUVECs)中血管内皮生长因子受体1型(VEGFR-1)和VEGFR-2细胞因子、磷酸肌肽3激酶(PI3k)和Ak菌株转化(Akt)蛋白表达水平的影响。结果,我们筛选了179个核心QRHXF抗血管生成靶点,包括血管内皮生长因子(VEGF)细胞因子。富集分析表明,56条核心信号通路中靶点富集,包括PI3k和Akt。体外实验表明,与诱导组相比,QRHXF组的迁移距离和平方、粘附光密度(OD)值以及成管分支点数量均显著减少(P
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Mechanism of Qingre Huoxue Fang treatment on inhibiting angiogenesis of rheumatoid arthritis based on network pharmacology and in vitro experiments.

This study aimed to explore the mechanism of Qingre Huoxue Fang (QRHXF) treatment on anti-angiogenesis in rheumatoid arthritis (RA) based on network pharmacology and in vitro experiments. We used the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and Therapeutic Target (TTD) database to extract the active components of QRHXF and potential targets for regulating angiogenesis. First, we used Cytoscape bioinformatics software to construct the network of QRHXF-angiogenesis and screened the potential targets. Then, we performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis on the potential core targets. In addition, enzyme-linked immune assay and Western blot were used for in vitro validation and to verify the effects of different concentrations of QRHXF on the expression levels of the vascular endothelial growth factor receptor type 1 (VEGFR-1) and VEGFR-2 cytokines and phosphoinositide 3-kinase (PI3k) and Ak strain transforming (Akt) proteins in human umbilical vein endothelial cells (HUVECs). In results, we screened 179 core QRHXF antiangiogenic targets, including vascular endothelial growth factor (VEGF) cytokines. Enrichment analysis showed that the targets were enriched in 56 core signaling pathways, including PI3k and Akt. In vitro experiments showed that the migration distance and square, adhesion optical density (OD) values, and the number of branch points in tube formation significantly decreased in the QRHXF group compared with the induced group (P<0.01). Notably, the serum levels of VEGFR-1 and VEGFR-2 were lower compared with the induced group (P<0.05 or P<0.01). In addition, the expressions of PI3K and p-Akt proteins were decreased in the middle- and high doses groups (P<0.01). This study's results suggest that the downstream mechanism of QRHXF anti-angiogenesis might inhibit the PI3K-Akt signalling pathway and downregulate VEGF-1 and VEGF-2.

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来源期刊
CiteScore
4.00
自引率
22.70%
发文量
0
审稿时长
6-12 weeks
期刊介绍: Journal of Physiology and Pharmacology publishes papers which fall within the range of basic and applied physiology, pathophysiology and pharmacology. The papers should illustrate new physiological or pharmacological mechanisms at the level of the cell membrane, single cells, tissues or organs. Clinical studies, that are of fundamental importance and have a direct bearing on the pathophysiology will also be considered. Letters related to articles published in The Journal with topics of general professional interest are welcome.
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