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1.山东中医药大学药学院,济南 250355
2.山东中医药高等专科学校中医系,山东 烟台 265200
3.山东中医药大学中医文献与文化研究院,济南 250355
4.山东中医药大学中医药经典理论教育部重点实验室,济南 250355
Received:09 January 2025,
Revised:2025-06-19,
Accepted:20 June 2025,
Published:30 July 2025
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赵明哲,王彬,赵晓旻,等.麻黄-桂枝药对对哮喘寒饮蕴肺证大鼠呼吸功能和气道炎症的影响及机制研究[J].中国药房,2025,36(14):1717-1721.
ZHAO Mingzhe,WANG Bin,ZHAO Xiaomin,et al.Effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism[J].ZHONGGUO YAOFANG,2025,36(14):1717-1721.
赵明哲,王彬,赵晓旻,等.麻黄-桂枝药对对哮喘寒饮蕴肺证大鼠呼吸功能和气道炎症的影响及机制研究[J].中国药房,2025,36(14):1717-1721. DOI: 10.6039/j.issn.1001-0408.2025.14.05.
ZHAO Mingzhe,WANG Bin,ZHAO Xiaomin,et al.Effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism[J].ZHONGGUO YAOFANG,2025,36(14):1717-1721. DOI: 10.6039/j.issn.1001-0408.2025.14.05.
目的
2
研究麻黄-桂枝药对对哮喘寒饮蕴肺证大鼠呼吸功能和气道炎症的影响及作用机制。
方法
2
将60只Wistar大鼠随机分为空白组、模型组、地塞米松组[1 mg/(kg·d)]和麻黄-桂枝低、中、高剂量组[0.234、0.936、1.872 g/(kg·d)],每组10只。模型组和各给药组大鼠通过腹腔注射抗原液(卵清蛋白100 mg+氢氧化铝100 mg)致敏、1%卵清蛋白雾化激发哮喘,并在此基础上施以“形寒、饮冷”刺激,建立哮喘寒饮蕴肺证大鼠模型。从实验第2天开始,各组大鼠灌胃相应药物或生理盐水,每天1次,连续给药21 d。观察各组大鼠在实验过程中的一般行为学变化,测定造模前和末次给药后的肺功能指标[呼气流量峰值(PEF)、气道阻力(Raw)、功能残气量(FRC)、呼气中期流速(EF50%)]以及末次给药后血清中白细胞介素6(IL-6)、IL-13、肿瘤坏死因子α(TNF-α)、干扰素γ(IFN-γ)含量,观察大鼠的肺组织病理学形态变化,检测其肺组织中IL-6、IL-13、TNF-α、IFN-γ、胸腺基质淋巴细胞生成素(TSLP)、Toll样受体4(TLR4)mRNA及TSLP、TLR4蛋白表达水平。
结果
2
与模型组比较,地塞米松组和麻黄-桂枝中、高剂量组大鼠肺组织损伤明显减轻;Raw,FRC,IL-6、IL-13、TNF-α含量及mRNA表达水平,TSLP、TLR4 mRNA及蛋白的表达水平均显著降低(
P
<0.05);PEF、EF50%和IFN-γ含量及mRNA表达水平均显著升高(
P
<0.05);只有少数大鼠出现哮喘典型症状。
结论
2
麻黄-桂枝药对能显著改善哮喘寒饮蕴肺证大鼠的呼吸功能,减轻气道炎症,其作用机制可能与抑制TSLP/TLR4信号通路、调节Th1/Th2失衡有关。
OBJECTIVE
2
To investigate the effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism.
METHODS
2
Sixty Wistar rats were randomly divided into blank group, model group, dexamethasone group [1 mg/(kg·d)], and Ephedra-Cinnamomum low-, medium-, high-dose groups [0.234, 0.936, 1.872 g/(kg·d)], with 10 rats in each group. The model and treatment groups were sensitized by intraperitoneal injection of antigen solution (ovalbumin 100 mg + aluminum hydroxide 100 mg) and challenged with 1% ovalbumin nebulization, along with exposure to a cold environment and ingestion of cold water, to establish the asthma model with cold-fluid retention in lung syndrome. From day 2, rats received corresponding drugs or normal saline intragastrically, once a day, for 21 consecutive days. The general behavioral changes in each group of rats were observed during the experimental process. The lung function parameters [peak expiratory flow (PEF), airway resistance (Raw), functional residual capacity (FRC), expiratory flow at 50% of forced vital capacity (EF50%)] were measured before modeling and after the last medication as well as serum contents of interleukin-6 (IL-6), IL-13, tumor necrosis factor-α (TNF-α) and interferon-gamma (IFN-γ) after the last medication were determined; the histopathological morphological changes in the lung tissues of rats were also observed; mRNA expressions of IL-6, IL-3, TNF-α, IFN-γ, thymic stromal lymphopoietin (TSLP), and Toll-like receptor 4 (TLR4), as well as protein expressions of TSLP and TLR4 were determined in lung tissue.
RESULTS
2
Compared with model group, the lung tissue damage of rats was relieved significantly; Raw, FRC, the contents and mRNA expression levels of IL-6, IL-13 and TNF-α, as well as the mRNA and protein expressions of TSLP and TLR4 were significantly decreased (
P
<0.05), while the contents and mRNA expressions of PEF, EF50 % and IFN-γ were significantly increased in the dexamethasone group and Ephedra-Cinnamomum medium- and high-dose groups (
P
<0.05). Moreover, only a few rats in the two groups exhibited typical symptoms of asthma.
CONCLUSIONS
2
Ephedra-Cinnamomum couplet medicinals improve respiratory function and ameliorate airway inflammation in asthma rats with cold-fluid retention in lung syndrome, the mechanism of which may be associated with inhibiting TSLP/TLR4 signaling pathway and modulating Th1/Th2 imbalance.
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