Improvement effect and mechanism of modified Jinfeicao powder on cough-variant asthma in rats
- VernacularTitle: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
- Author:
Jie CHEN
1
;
Qian SU
1
;
Chang LI
1
Author Information
1. Dept. of Pulmonology，Chongqing Hospital of the First Affiliated Hospital of Guangzhou University of Chinese Medicine （Chongqing Beibei Hospital of Traditional Chinese Medicine），Chongqing 400700，China
- Publication Type:Journal Article
- Keywords:
cough-variant asthma;
PI3K/AKT/mTOR pathway;
HIF-1α pathway;
oxidative stress;
airway inflammation;
airway remodeling
- From:
China Pharmacy
2026;37(17):2272-2278
- CountryChina
- Language:Chinese
-
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.
