Sodium houttuyfonate effectively alleviates benzoa pyrene-induced exacerbation of asthmatic airway inflammation in mice by inhibiting the IL-33-ST2/ERK pathway
10.3760/cma.j.cn112309-20241218-00431
- VernacularTitle:鱼腥草素钠通过抑制IL-33-ST2/ERK通路有效缓解苯并[a]芘暴露诱导的小鼠哮喘气道炎症加重
- Author:
Tao XU
1
;
Zhanling LIANG
;
Hui CAO
;
Xiaoyu LIU
;
Xiaojun XIAO
;
Liteng YANG
Author Information
1. 安徽理工大学医学院，淮南 232000
- Publication Type:Journal Article
- Keywords:
Benzo[a] pyrene;
Sodium houttuyfonate;
Asthma;
IL-33-ST2/ERK
- From:
Chinese Journal of Microbiology and Immunology
2025;45(4):332-340
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluatethe therapeutic efficacy and underlying mechanism of sodium houttuyfonate in treating airway inflammation in allergic asthma induced by co-exposure to the environmental pollutant benzo[a] pyrene (BaP) and ovalbumin (OVA).Methods:Thirty BALB/c mice were randomly divided into five groups with six mice in each group using a block randomization method: control, BaP, asthma model (OVA), BaP-exacerbated asthma (BaP+ OVA), and sodium houttuyfonate-treated BaP-exacerbated asthma (BaP+ OVA+ SH) groups. A mouse model of exacerbated asthma induced by co-exposure to BaP and OVA was established. Airway hyperresponsiveness, leukocyte distribution in bronchoalveolar lavage fluid (BALF), expression of cytokines such as IL-4, IL-13, IL-25, IL-33, thymic stromal lymphopoietin (TSLP) and IFN-γ, serum OVA-specific antibodies (IgE, IgG2a and IgG1), levels of malondialdehyde and superoxide dismutase (SOD) in lung tissues, and histopathological changes in lung tissues were evaluated. Western blot and RT-qPCR were used to detect the protein and mRNA expression levels of suppression of tumorigenicity 2 (ST2), extracellular regulated protein kinases (ERK), and phosphorylated ERK (p-ERK). Statistical analysis was conducted using analysis of variance and other statistical methods.Results:Compared with the BaP+ OVA group, the mice in the BaP+ OVA+ SH group showed significantly reduced airway hyperresponsiveness ( P<0.01), decreased numbers of total leukocytes ( P<0.01), neutrophils ( P<0.05), and lymphocytes ( P<0.01) in BALF, significantly downregulated secretion of IL-4, IL-13, IL-25, IL-33 and TSLP ( P<0.01), and inhibited production of IgE ( P<0.01) and IgG1 ( P<0.05). Additionally, sodium houttuyfonate treatment significantly decreased the malondialdehyde levels in lung tissues of mice with BaP-exacerbated asthma ( P<0.05) and reduced airway inflammatory cell infiltration, mucus secretion, and collagen fiber proliferation. Sodium houttuyfonate could supress the expression of ST2 and ERK ( P<0.05), inhibit ERK phosphorylation ( P<0.01), alleviate oxidative stress injury, and reduce collagen fiber proliferation in mouse lung tissues, thereby blocking the progression of BaP-exacerbated asthmatic inflammation. Conclusions:BaP exacerbates OVA-sensitized asthmatic airway inflammation in mice by inducing airway remodeling through the IL-33-ST2/ERK pathway. Sodium houttuyfonate inhibits this pathway, thereby preventing the progression of BaP-exacerbated asthma inflammation. This study provides new insights into the prevention and treatment of different phenotypes of asthma.
