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Updated: Jun 19, 2026

Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Elucidating the Potential Anti-asthmatic Mechanism of Aster tataricus by Combining Network Pharmacology with
Yun Zang1, Jia-Ning Zhang1, Si-Qi Yang1
1Institute of Pharmaceutical & Food Engineering, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Introduction:
Asthma is a prevalent chronic airway disease with unmet therapeutic needs. Aster tataricus L. f. (AT), a traditional herbal medicine used for respiratory conditions, shows potential for asthma treatment; however, its underlying pharmacological mechanisms remain largely unexplored. This study aimed to systematically investigate the potential therapeutic effects of AT against asthma and elucidate its underlying molecular mechanisms by integrating network pharmacology prediction, molecular docking validation, and in vivo experimental confirmation.
Methods:
To evaluate the anti-asthmatic potential of AT, an Ovalbumin (OVA)-induced murine model of allergic airway inflammation was employed. Pathological alterations in airway inflammation and remodeling were assessed via histochemistry (H&E, PAS, Masson's trichrome). Concurrently, the levels of key cytokines (IL-4, IL-5, IL-10, IL-13, IFN-γ) in Bronchoalveolar Lavage Fluid (BALF) were quantified by Enzyme-Linked Immunosorbent Assay (ELISA). Network pharmacology predictions and molecular docking analyses were integrated to identify potential targets and pathways, which were subsequently validated through Immunohistochemistry (IHC) and Immunofluorescence (IF).
Results:
In a murine model of allergic airway inflammation, AT treatment significantly alleviated airway inflammation and fibrosis. This therapeutic effect was characterized by a distinct shift in the BALF cytokines: a reduction in the levels of IL-4, IL-5, and IL-13, coupled with an elevation in IL-10 and IFN-γ. This shift was accompanied by diminished inflammatory cell infiltration and collagen deposition in lung tissue. Network pharmacology predicted core targets (e.g., EGFR, STAT3, TLR4, MMP9) and key pathways (e.g., PI3K-Akt and JAK-STAT). Experimental validation confirmed that AT downregulated the expression of these key targets. Furthermore, molecular docking revealed stable binding between active constituents in AT (such as Aster saponin F) and the core targets, suggesting a potential mechanism of action.
Discussion:
This study demonstrates the potential anti-asthmatic effects of AT in a murine model of allergic airway inflammation. The integrated research strategy reveals its multi-component synergistic mechanism of action.
Conclusions:
AT exerts potentially anti-asthmatic effects by means of multi-component and multi-target mechanisms, with the regulation of the PI3K-Akt and JAK-STAT pathways. This study elucidates the anti-asthmatic mechanism of AT and provides scientific evidence supporting its clinical application for asthma treatment.
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