程瑾,李杨,于艺薇,等.清膈煎对小鼠过敏性哮喘的治疗作用研究[J].中国海洋药物,2027,(2):-.
清膈煎对小鼠过敏性哮喘的治疗作用研究
The protective effect of Qingge Decoction on Allergic asthma in mice
投稿时间:2026-02-03  修订日期:2026-03-12
DOI:
中文关键词:  哮喘  清膈煎  NF-κB
English Keywords:Asthma  Qingge Decoction  NF-κB
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作者单位邮编
程瑾 中国海洋大学医药学院 266003
李杨 中国海洋大学医药学院 
于艺薇 中国海洋大学医药学院 
李海花 中国海洋大学医药学院 
卢玲 中国海洋大学医药学院 
郝杰杰* 中国海洋大学医药学院 
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中文摘要:
      摘 要:目的 研究经典名方清膈煎对卵清蛋白(OVA)诱导的哮喘小鼠的炎症、肺功能及其潜在分子机制的影响。方法 利用OVA诱导构建小鼠哮喘模型;给予不同浓度的清膈煎灌胃治疗,观察其对小鼠体质量及呼吸情况的影响;检测肺泡灌洗液(BALF)中炎症因子含量及炎症细胞的数量;利用苏木素-伊红(H&E)和阿利新蓝-过碘酸雪夫(AB-PAS)染色观察肺组织病理变化,通过转录组测序以及Western blot实验解析其核心调控通路。结果 清膈煎可以改善小鼠哮喘引起的体质量降低;可降低小鼠BALF中IL-4、IL-5、IL-6、IL-1β、IL-13的含量;降低血清中OVA-sIgE含量以及BALF中炎症细胞的数量;组织病理学检查显示,清膈煎治疗显著减轻了小鼠肺部炎症细胞聚集、杯状细胞增生和黏液分泌过多;Western blot结果显示,清膈煎能抑制NF-κB通路,从而发挥抗哮喘作用。结论 清膈煎能有效抑制OVA诱导的小鼠气道炎症与气道结构改变,改善肺功能,其机制可能与靶向抑制NF-κB信号通路有关。
English Summary:
      Abstract: Objective To investigate the effects of the classical formula Qingge Decoction on inflammation, pulmonary function, and underlying molecular mechanisms in ovalbumin (OVA)-induced asthmatic mice. Methods An OVA-induced mouse asthma model was established; administered Qingge Decoction at varying concentrations via oral gavage to observe effects on body weight, respiratory status, inflammatory cytokine levels in bronchoalveolar lavage fluid (BALF), and inflammatory cell counts; examined pulmonary histopathology using H&E and AB-PAS staining; and analysed core regulatory pathways via transcriptome sequencing and Western blot analysis. Results Qingge Decoction ameliorated asthma-induced weight loss in mice; reduced levels of IL-4, IL-5, IL-6, IL-1β, and IL-13 in BALF; decreased serum OVA-sIgE levels and inflammatory cell counts in BALF; histopathological examination revealed that Qingge Decoction treatment significantly alleviated pulmonary inflammatory cell aggregation, goblet cell hyperplasia, and excessive mucus secretion; Western blot analysis demonstrated that Qingge Decoction inhibits the NF-κB pathway, thereby exerting anti-asthmatic effects. Conclusion Qingge Decoction effectively suppresses OVA-induced airway inflammation and structural alterations in mice, improving pulmonary function. Its mechanism may involve targeted inhibition of the NF-κB signalling pathway.
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