Effects of atractylodin on lung injury and airway inflammation in rats with AECOPD by regulating JNK/p38 MAPK signaling pathway
- VernacularTitle:苍术素调节JNK/p38MAPK信号通路对AECOPD大鼠肺损伤和气道炎症的影响
- Author:
Zhiying SUN
1
;
Yingzhe WANG
2
;
Yuan LIU
3
;
Yapeng ZHAO
1
;
Tingting ZHOU
4
Author Information
1. Dept. of Critical Care Medicine （Ⅱ），Hebei Provincial Hospital of Traditional Chinese Medicine，Shijiazhuang 050011，China
2. Dept. of Respiratory and Critical Care Medicine Ⅱ，Hebei Provincial Hospital of Traditional Chinese Medicine，Shijiazhuang 050011，China
3. Dept. of Critical Care Medicine，Hebei Provincial Hospital of Traditional Chinese Medicine，Shijiazhuang 050011，China
4. Dept. of Respiratory Critical Care，Hebei Provincial Hospital of Traditional Chinese Medicine，Shijiazhuang 050011，China
- Publication Type:Journal Article
- Keywords:
atractylodin;
acute exacerbation of chronic obstructive pulmonary disease;
lung injury;
airway inflammation;
JNK/
- From:
China Pharmacy
2025;36(23):2935-2940
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To discuss the effect mechanism of atractylodin （ATR） on lung injury and airway inflammation in rats with acute exacerbation of chronic obstructive pulmonary disease （AECOPD）. METHODS AECOPD model was established using smoke exposure and intratracheal injection of lipopolysaccharide. Rats were randomly grouped into model group， ATR low-， medium- and high-dose groups （25， 50 and 100 mg/kg）， as well as high-dose ATR+anisomycin [ANS， c-Jun N-terminal kinase （JNK） activator] group （100 mg/kg ATR+5 mg/kg ANS）. Additionally， a non-modeled control group was set up， with 12 rats in each group. Rats in each group were intraperitoneally injected with the corresponding drug solution/normal saline once daily for 14 consecutive days. After the last medication， lung function [peak expiratory flow （PEF）， the ratio of forced expiratory volume （FEV） to forced vital capacity （FVC）， arterial partial pressure of oxygen （PaO2）]， as well as the number of inflammatory cells and the levels of inflammatory cytokines [interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and IL-1β] in bronchoalveolar lavage fluid （BALF）， were measured. The pathological morphology of lung tissue in rats was observed. 163.com The apoptosis of lung epithelial cells was detected， and the expression levels of proteins related to the JNK/p38 mitogen-activated protein kinase （p38 MAPK） signaling pathway in rat lung tissues were detected. RESULTS Compared with control group， PEF， FEV/FVC and PaO2 of model group were slowed or decreased significantly （P＜0.05）. The number of white blood cells， neutrophils， lymphocytes and macrophages， as well as the levels of IL-1β， TNF-α and IL-6 in BALF， along with the pathological score， the apoptosis rate of lung epithelial cells， and the phosphorylation levels of JNK and p38 MAPK proteins in lung tissues， were all increased or raised significantly （P＜0.05）； lung tissue exhibited severe damage， with disordered cell arrangement and marked infiltration of inflammatory cells. Compared with model group， the levels of above quantitative indicators in rats from all ATR dosage groups showed significant improvement in a dose-dependent manner （P＜0.05）； moreover， the pathological damage in lung tissue was alleviated， with cells arranged in a regular and orderly fashion. Compared with ATR high-dose group， the levels of the above quantitative indicators in rats from the high-dose ATR+ANS group were significantly reversed （P＜0.05）， and the pathological damage in lung tissue was exacerbated. CONCLUSIONS ATR inhibits airway inflammation by suppressing the activity of the JNK/p38 MAPK signaling pathway， thereby improving lung tissue damage in AECOPD rats.
