Background

This study aimed to explore the underlying anti-asthma pharmacological mechanisms of conciliatory anti-allergic decoction (CAD) with a network pharmacology approach.

Methods

Traditional Chinese medicine related databases were utilized to screen the active ingredients of CAD. Targets of CAD for asthma treatment were also identified based on related databases. The protein-protein interaction network, biological function and KEGG pathway enrichment analysis, and molecular docking of the targets were performed. Furthermore, an asthma mouse model experiment involving HE staining, AB-PAS staining, and ELISA was also performed to assess the anti-asthma effect of CAD.

Results

There were 77 active ingredients in CAD, including quercetin, kaempferol, stigmasterol, luteolin, cryptotanshinone, beta-sitosterol, acacetin, naringenin, baicalin, and 48 related targets for asthma treatment, mainly including TNF, IL4, IL5, IL10, IL13 and IFN-γ, were identified with ideal molecular docking binding scores by network pharmacology analysis. KEGG pathway analysis revealed that these targets were directly involved in the asthma pathway, Th1 and Th2 cell differentiation, and signaling pathways correlated with asthma (NF-κB, IL17, T cell receptor, TNF, JAK-STAT signaling pathways, etc.). Animal experiments also confirmed that CAD could attenuate inflammatory cell invasion, goblet cell hyperplasia and mucus secretion. The levels of the major targets TNF-α, IL4, IL5, and IL13 can also be regulated by CAD in an asthma mouse model.

Conclusion

The anti-asthma mechanism of CAD possibly stemmed from the active ingredients targeting asthma-related targets, which are involved in the asthma pathway and signaling pathways to exhibit therapeutic effects.

中文翻译：

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基于网络药理学的调和抗过敏汤对哮喘保护机制的研究。

背景

本研究旨在通过网络药理学方法探索调和抗过敏汤（CAD）的潜在抗哮喘药理机制。

方法

利用中药相关数据库筛选CAD的有效成分。还根据相关数据库确定了用于哮喘治疗的CAD对象。进行了蛋白质-蛋白质相互作用网络，生物学功能和KEGG途径富集分析，以及靶标的分子对接。此外，还进行了涉及HE染色，AB-PAS染色和ELISA的哮喘小鼠模型实验，以评估CAD的抗哮喘作用。

结果

CAD中有77种有效成分，包括槲皮素，山奈酚，豆甾醇，木犀草素，隐丹参酮，β-谷甾醇，醋西西汀，柚皮苷，黄ical苷和48种哮喘相关靶标，主要包括TNF，IL4，IL5，IL10，IL13和IFN。 -γ，通过网络药理分析具有理想的分子对接结合分数。KEGG通路分析显示，这些靶标直接参与哮喘通路，Th1和Th2细胞分化以及与哮喘相关的信号通路（NF-κB，IL17，T细胞受体，TNF，JAK-STAT信号通路等）。动物实验还证实，CAD可以减轻炎症细胞的侵袭，杯状细胞的增生和粘液分泌。在哮喘小鼠模型中，主要靶标TNF-α，IL4，IL5和IL13的水平也可以通过CAD进行调节。

结论

CAD的抗哮喘机制可能源于靶向哮喘相关靶标的活性成分，这些活性成分参与哮喘途径和信号传导途径以发挥治疗作用。