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沙参叶挥发油对哮喘气道炎症的疗效和机制:网络药理学和体内研究

2022/01/28

   摘要
   背景:哮喘是最常见的气道慢性炎症性疾病之一。据报道,沙松叶精油(EOA)具有抗炎作用。本研究旨在通过网络分析预测EOA对哮喘的抑制作用,并确认EOA对气道炎症的潜在机制。
   目的和研究设计:通过电子网络药理学和体内实验研究,研究EOA对哮喘的作用和潜在机制。
   方法:使用EOA的主要成分构建网络药理学,以确定EOA对哮喘的有效性。EOA(0.0003和0.03 v/v%)通过雾化器雾化,每周3次,每次5分钟,持续7周。用EOA治疗小鼠3周后,用卵清蛋白(OVA)和PM10致敏小鼠,诱发哮喘。EOA对IL-17相关信号通路的影响通过哮喘模型得到证实。
   结果:网络分析显示EOA与IL-17相关的信号通路高度相关。EOA抑制肺和气管组织中的呼吸道上皮增生、胶原沉积和杯状细胞活化。此外,EOA减少BALF中嗜酸性粒细胞、淋巴细胞和巨噬细胞的数量。此外,在小鼠哮喘模型中,我们发现EOA抑制IL-17相关细胞因子,增加Treg相关细胞因子,降低TRAF6和MAPK,抑制NF-kB的核转录活性。
   结论:网络药理学和体内研究表明,EOA可能通过IL-17相关信号通路抑制哮喘暴露时的气道炎症。
 
 
(中日友好医院呼吸与危重症医学科 顾宪民 摘译 林江涛 审校)
(Phytomedicine.2021 Dec 24;96:153898.doi: 10.1016/j.phymed.2021.153898.)
 

 
Efficacy and mechanism of essential oil from Abies holophylla leaf on airway inflammation in asthma: Network pharmacology and in vivo study
 
Nayoung Park, Sang Jun Park, Mi Hye Kim, Woong Mo Yang
 
Abstract
BACKGROUND: Asthma is one of the most common chronic inflammatory diseases of the airways. Essential oil from Abies holophylla leaf (EOA) has been reported to have anti-inflammatory property. This study aimed to predict the inhibitory effect of EOA against asthma by network analysis and to confirm the underlying mechanism of EOA on airway inflammation.
PURPOSE AND STUDY DESIGN: The effects and underlying mechanisms of EOA on asthma were investigated by in silico network pharmacology and an experimental in vivo study.
METHODS: To define the effectiveness of EOA on asthma, the network pharmacology was constructed using major components of EOA. EOA (0.0003 and, 0.03 v/v%) was aerosolized by nebulizer 3 times a week for 5 min for 7 weeks. After 3 weeks of treating the mice with EOA, asthma was induced by sensitizing them with ovalbumin (OVA) and PM10. The effects of EOA on the IL-17 related signaling pathway was confirmed using an asthmatic model.
RESULTS: The network analysis showed that EOA is highly associated with the IL-17-related signaling pathway. EOA inhibited respiratory epithelium hyperplasia, collagen deposition and goblet cell activation in the lung and trachea tissues. In addition, EOA reduced the number of eosinophils, lymphocytes and macrophages in BALF. Furthermore, in the asthmatic model of mice, we showed that EOA inhibited IL-17-related cytokines, increased Treg-related cytokines and decreased the TRAF6 and MAPK and, suppressed the nuclear transcriptional activities of NF-kB.
CONCLUSIONS: The network pharmacology and in vivo study indicated that EOA may have an inhibitory effect on airway inflammation in asthma exposure through the IL-17-related signaling pathway.
 


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