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加减金沸草散对咳嗽变异性哮喘模型大鼠的改善作用及机制
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| 篇名： | 加减金沸草散对咳嗽变异性哮喘模型大鼠的改善作用及机制 |
| TITLE： | Improvement effect and mechanism of modified Jinfeicao powder on cough-variant asthma in rats |
| 摘要： | 目的 探讨加减金沸草散（MJCP）对咳嗽变异性哮喘（CVA）模型大鼠的改善作用及机制。方法采用网络药理学挖掘MJCP治疗CVA的关键靶点及信号通路。将大鼠分为正常对照组、模型组、阳性对照组（醋酸泼尼松，0.9mg/kg）和MJCP低、中、高剂量组（3.5、7、14g/kg），每组6只。除正常对照组外，其余各组大鼠均构建CVA模型。从实验第14天起，各组大鼠灌胃相应药物/生理盐水，每天1次，持续14d。末次给药后，检测/观察大鼠咳嗽次数、血清中免疫炎症与氧化应激相关指标水平、肺组织病理形态学变化及相关通路蛋白表达。结果网络药理学挖掘出肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、蛋白激酶B（AKT）等5个关键靶点以及磷脂酰肌醇3-激酶（PI3K）/AKT/哺乳动物雷帕霉素靶蛋白（mTOR）、缺氧诱导因子1α（HIF-1α）等通路。动物实验结果显示，与模型组相比，各给药组大鼠咳嗽次数均显著减少（P＜0.05）；血清中免疫球蛋白E（IgE）、IL-6、TNF-α、Src家族酪氨酸蛋白激酶、表皮生长因子受体、丙二醛（MDA）水平（MJCP低剂量组IgE、MDA除外），平均病理评分，气道壁总面积/支气管基底膜周长值，肺组织中α-平滑肌肌动蛋白、Ⅰ型胶原蛋白表达水平和PI3K、AKT（MJCP低剂量组除外）、mTOR蛋白磷酸化水及HIF-1α蛋白表达水平均显著降低（P＜0.05）；血清中谷胱甘肽（MJCP低剂量组除外）、超氧化物歧化酶水平均显著升高（P＜0.05）。结论MJCP可通过调控PI3K/AKT/mTOR和HIF-1α通路，抑制气道炎症与气道重塑、调节氧化应激，从而发挥对CVA的改善作用。 |
| ABSTRACT： | OBJECTIVE To investigate the improvement effect and mechanism of modified Jinfeicao powder （MJCP） on cough-variant asthma （CVA） in rats.METHODS Network pharmacology was employed to identify the key targets and signaling pathways involved in the therapeutic action of MJCP against CVA. Rats were divided into normal control group， model group， positive control group （prednisone acetate， 0.9 mg/kg）， and MJCP low-， medium-， and high-dose groups （3.5， 7， 14 g/kg）， with six rats in each group. Except for the normal control group， CVA models were established in other groups. From day 14 of the experiment， rats in each group were administered corresponding drugs or normal saline intragastrically once daily for 14 consecutive days. After the final administration， cough frequency， serum levels of immune-inflammatory and oxidative stress-related indicators， pulmonary histopathological changes， and expression of pathway-related proteins were detected and observed.RESULTS Network pharmacology identified five key targets， including tumor necrosis factor-α （TNF-α）， interleukin-6（IL-6）， and protein kinase B（AKT）， as well as signaling pathways such as phosphatidylinositol 3-kinase （PI3K）/AKT/mammalian target of rapamycin （mTOR） and hypoxia-inducible factor-1α （HIF-1α）. Animal experimental results showed that， compared with the model group， cough frequency was significantly reduced in all treatment groups （ P ＜0.05）. Serum levels of immunoglobulin E （IgE）， IL-6， TNF-α， Src family of protein tyrosine kinase， epidermal growth factor receptor， and malondialdehyde （MDA） （except for IgE and MDA in the MJCP low-dose group）， mean pathological scores， the ratio of total airway wall area to basement membrane perimeter， and the expression levels of α -smooth muscle actin， Collagen-Ⅰ， phosphorylated PI3K， phosphorylated AKT （except in the MJCP low-dose group）， phosphorylated mTOR， and HIF-1α protein in lung tissues were all significantly decreased （ P ＜0.05）. Glutathione （except in the MJCP low-dose group） and superoxide dismutase levels in serum were significantly increased（ P ＜0.05）.CONCLUSIONS MJCP may alleviate airway inflammation， airway remodeling， and oxidative stress by regulating the PI3K/AKT/mTOR and HIF-1α signaling pathways， thereby exerting its improvement effects on CVA. |
| 期刊： | 2026年第37卷第17期 |
| 作者： | 陈洁；苏倩；李常 |
| AUTHORS： | CHEN Jie，SU Qian，LI Chang |
| 关键字： | 加减金沸草散；咳嗽变异性哮喘；PI3K/AKT/mTOR通路；HIF-1α通路；氧化应激；炎症反应；气道重塑 |
| KEYWORDS： | cough-variant asthma;PI3K/AKT/mTOR pathway;HIF-1α pathway;oxidative stress;airway inflammation;airway remodeling |
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