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Biochanin A attenuates ovalbumin-induced airway inflammation in asthmatic rats by regulating TLR4/NF-κB/NLRP3 signaling pathway
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DOI   10.11656/j.issn.1672-1519.2023.04.17
Key Words   biochanin A;toll-like receptor 4/nuclear factor-κB/NOD-like receptor protein 3 signaling pathway;asthma;airway inflammation
Author NameAffiliationE-mail
QI Shasha Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China  
LYU Minying Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China  
FU Xiaomei Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China  
ZHANG Guowei Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China  
ZHANG Hong Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China  
ZHANG Xuya Department of Pediatrics, The First Affiliated Hospital of Henan University, Kaifeng 475100, China zhangxy1819@126.com 
Abstract
    [Objective] To investigate the impact of biochanin A (BCA) on ovalbumin (OVA)-induced airway inflammation in asthmatic rats by regulating Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB)/NOD-like receptor protein 3 (NLRP3) signaling pathway. [Methods] SD rats were divided into control check(CK)group, model group, low-dose BCA group (BCA-L group, 25 mg/kg), high-dose BCA group(BCA-H group, 100 mg/kg), and dexamethasone positive control group(Dex group, 1 mg/kg), and BCA-H+LPS (TLR4 activator) group (100 mg/kg+0.1 mg/kg), 12 rats in each group. Except for the CK group, other groups were induced by OVA to establish the asthmatic rat model. After 24 hours of successful modeling, drug treatment was carried out, and the drug was administered once a day for 10 d. The changes of inspiratory resistance, expiratory resistance and lung ventilation compliance of rats were detected by animal lung function analyzer;Giemsa staining was used to detect the total number of cells, and the numbers of lymphocytes, eosinophils and neutrophils in bronchoalveolar lavage fluid(BALF). ELISA was used to detect the levels of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β) and interferon-γ(IFN-γ) in BALF;HE staining was used to detect the pathological changes of rat lung tissue;immunohistochemistry was used to detect the expression of eosinophil chemokine (Eotaxin) in rat lung tissue;Western blot was used to detect the protein expressions of TLR4, p-NF-κB p65 and NLRP3 in rat lung tissue. [Results] Compared with the CK group, inspiratory resistance, expiratory resistance, the total number of cells, the numbers of lymphocytes, eosinophils, neutrophils, the levels of TNF-α, IL-1β, and IFN-γ in the BALF of the Model group increased, and the infiltration of inflammatory cells around the bronchi and blood vessels in the lung tissue was obvious, the percentage of Eotaxin positive staining area, and the protein expressions of TLR4, p-NF-κB p65 and NLRP3 in lung tissue increased, reduced lung ventilation compliance (P<0.05);Compared with the Model group, the corresponding indicators of the BCA-L group, BCA-H group and Dex group had the opposite trends(P<0.05);LPS attenuated the ameliorating effect of high-dose BCA on airway inflammation in asthmatic rats. [Conclusion] BCA may alleviate airway inflammation in OVA-induced asthmatic rats by inhibiting TLR4/NF-κB/NLRP3 signaling pathway.

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