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The Journal of asthma : official journal of the Association for the Care of Asthma · 2026

Exploring the mechanism of Zhichuanling oral liquid in treating childhood bronchial asthma based on network pharmacology and experimental verification.

СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Wang Jiao, Li Jiaxin, Wang Xianhe, Zhang Lihai, Liu Qiuyan, Yang Duo

Аннотация

BACKGROUND: Bronchial asthma (BA), a common chronic airway inflammatory disease, significantly impairs lung function and quality of life due to pathological features such as airway remodeling, inflammatory imbalance, and oxidative damage. This study aimed to investigate the clinical efficacy of Zhichuanling Oral Liquid (ZCL) in children with BA and elucidate its mechanism of action through network pharmacology, animal experiments, and cellular studies.

METHODS: Sixty children with BA were randomly divided into a control group (conventional treatment) and an observation group (+ZCL). Clinical efficacy, lung function, and serum markers (IL-6, SAA, and IgE) were evaluated. Network pharmacology identified potential targets and pathways. An OVA-induced BA mouse model and cultured airway smooth muscle cells (ASMCs) were used to validate the mechanism.

RESULTS: Results showed ZCL significantly improved lung function (FVC, FEV1, and PEF), reduced symptom scores, and decreased IL-6, SAA, and IgE levels compared to control. Symptom relief times were shorter, and overall effective rate was higher (86.67% vs 60.00%). Network pharmacology revealed core targets (NFKB1, SIRT1, HIF1A, and MMP9) and component QCT, involving IL-17 pathway. In mice, ZCL reduced behavioral scores, IL-17, IL-4, MDA, and increased SOD, GSH-Px, alleviating airway inflammation. Medium-dose ZCL was most effective. In ASMCs, ZCL upregulated SIRT1, reduced NF-κB, IL-17, and oxidative stress, enhanced by SIRT1 overexpression.

CONCLUSIONS: ZCL effectively treats childhood BA, as demonstrated by improvements in lung function and symptoms. Its mechanism is likely mediated by QCT regulating the SIRT1/NF-κB/IL-17 pathway to reduce airway inflammation and oxidative damage.

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