Immunopharmacology and immunotoxicology · 2025
Immunomodulatory and anti-apoptotic effects of pediatric anti-cough and asthma sirup in mice with cigarette smoke extract-induced asthma.
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Zhang Qiong, Jiang Yang
Аннотация
BACKGROUND: Asthma, a chronic inflammatory disease characterized by inflammation and immunological abnormalities, was the focus of this study, which explored the mechanisms and efficacy of a pediatric anti-cough and asthma sirup in a cigarette smoke extract (CSE)-induced rat asthma model.
METHODS: A CSE-induced asthma rat model was treated with a sirup containing roasted ephedra, bitter almond, gypsum, and licorice. Key markers in serum/BALF were measured by ELISA. Inflammatory cells were analyzed by Giemsa staining, pathology by hematoxylin-eosin, and macrophage infiltration by CD68+ immunohistochemistry. Lung tissue apoptosis (TUNEL), and apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-3) plus phosphorylated NF-κB (all by Western blot) were evaluated.
RESULTS: The sirup treatment significantly attenuated CSE-induced airway inflammation in asthmatic rats, shown by decreased serum IL-4, IL-5, and IL-13, and reduced inflammatory cell infiltration in BALF. It also restored oxidative balance by reversing MDA elevation and SOD reduction. Histopathologically, it alleviated peribronchial inflammation, cell infiltration, hemolysis, and alveolar septum thickening. Furthermore, it suppressed CSE-induced lung apoptosis, evidenced by fewer TUNEL-positive cells, reduced pro-apoptotic proteins (Bax and cleaved caspase-3), and increased anti-apoptotic Bcl-2, likely via inhibiting NF-κB pathway activation.
CONCLUSION: The pediatric sirup holds therapeutic potential against CSE-induced asthma by regulating cytokine levels and decreasing pulmonary inflammation/apoptosis.
METHODS: A CSE-induced asthma rat model was treated with a sirup containing roasted ephedra, bitter almond, gypsum, and licorice. Key markers in serum/BALF were measured by ELISA. Inflammatory cells were analyzed by Giemsa staining, pathology by hematoxylin-eosin, and macrophage infiltration by CD68+ immunohistochemistry. Lung tissue apoptosis (TUNEL), and apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-3) plus phosphorylated NF-κB (all by Western blot) were evaluated.
RESULTS: The sirup treatment significantly attenuated CSE-induced airway inflammation in asthmatic rats, shown by decreased serum IL-4, IL-5, and IL-13, and reduced inflammatory cell infiltration in BALF. It also restored oxidative balance by reversing MDA elevation and SOD reduction. Histopathologically, it alleviated peribronchial inflammation, cell infiltration, hemolysis, and alveolar septum thickening. Furthermore, it suppressed CSE-induced lung apoptosis, evidenced by fewer TUNEL-positive cells, reduced pro-apoptotic proteins (Bax and cleaved caspase-3), and increased anti-apoptotic Bcl-2, likely via inhibiting NF-κB pathway activation.
CONCLUSION: The pediatric sirup holds therapeutic potential against CSE-induced asthma by regulating cytokine levels and decreasing pulmonary inflammation/apoptosis.