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Protective effect of amygdalin on epithelial–mesenchymal transformation in experimental chronic obstructive pulmonary disease mice
Author(s) -
Wang Ziyan,
Fang Keyong,
Wang Guoqiang,
Guan Xuewa,
Pang Zhiqiang,
Guo Yingqiao,
Yuan Yuze,
Ran Nan,
Liu Yue,
Wang Fang
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6274
Subject(s) - amygdalin , copd , medicine , immunohistochemistry , vimentin , epithelial–mesenchymal transition , lung , western blot , oleanolic acid , pathology , pulmonary fibrosis , immunology , fibrosis , pharmacology , biology , biochemistry , cancer , alternative medicine , gene , metastasis
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.