基于网络药理学阐明咳喘六味合剂治疗重症哮喘的作用机制和分子靶点。

Yanqi Cheng, Ding Sun, Lu Zou, Shaobin Li, Ling Tang, Xiao Yu, Binqing Tang, Yingen Wu, Hong Fang
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引用次数: 1

摘要

咳喘六味合剂是治疗严重哮喘的常用中药方剂。然而,KCLW的潜在治疗机制尚不清楚。本研究采用网络药理学方法,通过TCMSP数据库和超高效液相色谱-飞行时间质谱联用,对KCLW的化学成分进行了鉴定。采用差异表达鉴定、蛋白质-蛋白质相互作用(PPI)网络和功能富集分析筛选KCLW治疗严重哮喘的关键靶点。我们的研究结果证实,槲皮素、木犀草素、山奈酚和汉黄芩素是KCLW中最关键的活性成分。此外,通过重叠KCLW推定靶标和严重哮喘相关基因的PPI网络,获得了KCLW的16个相关严重哮喘相关靶标,其中最重要的靶标是IL-6、NOS2、VEGFA、CXCL2和PLAT。在功能上,16个靶点及其相互作用的差异表达基因主要与免疫和炎症相关的生物学功能和途径有关,如炎症反应、T细胞分化、Nrf2/HO-1信号通路、TGF-β/Smad信号通路和NF-κB信号通路。KCLW抑制PDGF BB诱导的气道平滑肌细胞的炎症。总之,本研究揭示了KCLW治疗严重哮喘的活性物质及其潜在的治疗机制,为KCLW对抗严重哮喘提供了临床指导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Elucidation of the mechanisms and molecular targets of KeChuanLiuWei-Mixture for treatment of severe asthma based on network pharmacology

Elucidation of the mechanisms and molecular targets of KeChuanLiuWei-Mixture for treatment of severe asthma based on network pharmacology

KeChuanLiuWei-Mixture (KCLW) is widely used as a Chinese medicine prescription to treat severe asthma. However, the underlying therapeutic mechanism of KCLW remains unclear. In this study, a network pharmacology method was used to identify the chemical constituents of KCLW by the TCMSP database and ultra-performance liquid chromatography coupled with time-of-flight mass spectrometry. Differential expression identification, protein–protein interaction (PPI) network and functional enrichment analysis were used to screen key targets of KCLW for severe asthma. Our results confirmed that quercetin, luteolin, kaempferol, and wogonin are the most critical active ingredients in KCLW. Moreover, the 16 relevant severe asthma-related targets of KCLW were obtained by overlapping the PPI networks of the KCLW putative targets and severe asthma-related genes, among which the most important targets were IL-6, NOS2, VEGFA, CXCL2, and PLAT. Functionally, the 16-targets and their interacting differentially expressed genes were primarily related to biological functions and pathways related to immunity and inflammation, such as inflammatory response, T cell differentiation, Nrf2/HO-1 signaling pathway, TGF-β/Smad signaling pathway, and NF-κB signaling pathway. KCLW inhibited inflammation in PDGF-BB-induced airway smooth muscle cells. In summary, this study demonstrates the active substance and potential therapeutic mechanism of KCLW in severe asthma, and offers a clinical direction for KCLW against severe asthma.

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