Protective effect of amygdalin on epithelial–mesenchymal transformation in experimental chronic obstructive pulmonary disease mice

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory pulmonary disease characterized by continuous, progressive limitation of airflow. Airway remodelling, which is correlated with epithelial–mesenchymal transitions (EMTs), is a typical pathophysiological change of COPD. Amygdalin,...

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Bibliographic Details
Published in:Phytotherapy research 2019-03, Vol.33 (3), p.808-817
Main Authors: Wang, Ziyan, Fang, Keyong, Wang, Guoqiang, Guan, Xuewa, Pang, Zhiqiang, Guo, Yingqiao, Yuan, Yuze, Ran, Nan, Liu, Yue, Wang, Fang
Format: Article
Language:English
Subjects:
Air flow
amygdalin
Amygdalin - pharmacology
Animals
Cells, Cultured
Chronic obstructive pulmonary disease
Cigarette smoke
Disease control
E-cadherin
Enzyme-linked immunosorbent assay
Epithelial cells
Epithelial-Mesenchymal Transition - drug effects
epithelial–mesenchymal transition
Female
Fibrosis
Genetic transformation
Herbal medicine
Humans
Lung - metabolism
Lung diseases
Male
Mesenchyme
Mice
Mice, Inbred BALB C
Morphology
Obstructive lung disease
Pharmacology
Pulmonary Disease, Chronic Obstructive - drug therapy
Pulmonary Disease, Chronic Obstructive - metabolism
Pulmonary Disease, Chronic Obstructive - pathology
Respiratory tract
Smad2 protein
Smad2 Protein - metabolism
Smad3 Protein - analysis
Smoke
TGF‐β1
Tissues
Traditional Chinese medicine
Transforming Growth Factor beta1 - analysis
Transforming growth factor-b1
Vimentin
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Summary:Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory pulmonary disease characterized by continuous, progressive limitation of airflow. Airway remodelling, which is correlated with epithelial–mesenchymal transitions (EMTs), is a typical pathophysiological change of COPD. Amygdalin, an active ingredient in the traditional Chinese medicine bitter almond with extensive pharmacological effects, was shown to inhibit tissue fibrosis in recent studies. In this study, a human bronchial epithelial cell line (BEAS‐2B) and mice were exposed to cigarette smoke, and EMT levels were investigated after treatment with different concentrations of amygdalin. Morphology was assessed by immunohistochemical staining. Evaluation of the expression of TGF‐β1, smad2/3, and p‐smad2/3 in lung tissue was conducted out via ELISA, Western blot, and real‐time PCR. The results showed that E‐cadherin expression was significantly increased, whereas vimentin, TGF‐β1, and phosphorylated smad2/3 (p‐smad2/3) expression was markedly decreased in the amygdalin‐treated groups compared with the model group. Therefore, our study demonstrated a protective role of amygdalin in the murine EMT process after COPD.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.6274