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基于网络药理学的干脊龙治疗腰痛机制解析。

Network Pharmacology-Based Dissection of the Mechanism of Drynariae Rhizoma for Low Back Pain.

机构信息

Hubei University of Chinese Medicine, Wuhan 430061, China.

Affiliated Hospital of Hubei University of Chinese Medicine, Wuhan 430061, China.

出版信息

Biomed Res Int. 2022 Oct 17;2022:6092424. doi: 10.1155/2022/6092424. eCollection 2022.

Abstract

OBJECTIVE

To explain the potential mechanisms of Drynariae Rhizoma (DR) in the treatment of low back pain (LBP).

DESIGN

Network pharmacology was used to reveal the potential mechanisms including collecting the active ingredients of DR, analyzing the common gene targets of LBP and DR, constructing protein-protein interaction (PPI) network, collecting protein classification, performing Gene Ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and verifying significant gene targets.

RESULTS

234 different gene targets and 18 active compounds altogether were obtained. AKT1, VEGFA, and HIF1A were deemed to be major gene targets based on the degree values. According to GO analysis, steroid metabolic process involved 42 (18.10%) potential therapeutic LBP targets, neuronal cell body involved 24 (10.30%) potential therapeutic LBP targets, and protein serine/threonine kinase activity involved 28 (12.02%) potential therapeutic LBP targets in biological process (BP), cellular component (CC), and molecular function (MF), respectively. According to KEGG and pathway interaction analyses, the PI3K-Akt signaling pathway involved 34 (15.89%) potential therapeutic LBP targets, and PI3K-Akt signaling pathway played a significant role in the treatment of LBP. The mRNA expression levels of AKT1 and HIF1A were upregulated in healthy nucleus pulposus (NP) tissue than in degenerative NP tissue. In contrast, the mRNA expression level of VEGFA was downregulated in healthy NP tissue than in degenerative NP tissue.

CONCLUSIONS

In this study, we identified a potential relationship between LBP and DR in this work, as well as a synergistic mechanism of DR in the treatment of LBP, which serves as a benchmark for further in vivo and in vitro research.

摘要

目的

阐释骨碎补治疗腰痛(LBP)的潜在作用机制。

设计

采用网络药理学方法,收集骨碎补的活性成分,分析 LBP 和骨碎补的共同基因靶点,构建蛋白质-蛋白质相互作用(PPI)网络,收集蛋白分类,进行基因本体(GO)功能分析和京都基因与基因组百科全书(KEGG)通路富集分析,并验证显著的基因靶点。

结果

共获得 234 个不同的基因靶点和 18 个活性化合物。根据度值,AKT1、VEGFA 和 HIF1A 被视为主要的基因靶点。根据 GO 分析,类固醇代谢过程涉及 42 个(18.10%)潜在的治疗 LBP 靶点,神经元细胞体涉及 24 个(10.30%)潜在的治疗 LBP 靶点,蛋白丝氨酸/苏氨酸激酶活性涉及 28 个(12.02%)潜在的治疗 LBP 靶点,分别在生物过程(BP)、细胞成分(CC)和分子功能(MF)中。根据 KEGG 和通路相互作用分析,PI3K-Akt 信号通路涉及 34 个(15.89%)潜在的治疗 LBP 靶点,PI3K-Akt 信号通路在治疗 LBP 中发挥重要作用。与退变的椎间盘相比,健康椎间盘组织中 AKT1 和 HIF1A 的 mRNA 表达上调,而 VEGFA 的 mRNA 表达下调。

结论

在这项研究中,我们确定了 LBP 和骨碎补之间的潜在关系,以及骨碎补治疗 LBP 的协同作用机制,为进一步的体内和体外研究提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca58/9592205/e7fa357f1bd6/BMRI2022-6092424.001.jpg

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