Open AccessAnti-inflammatory effects of potato extract on a rat model of cigarette smoke–induced chronic obstructive pulmonary disease
Author(s) -
Gui Hua Xu,
Jie Shen,
Peng Sun,
Min Yang,
Peng Zhao,
Yan Niu,
Jing Lu,
Zhi Qiang Wang,
Chao Gao,
Hongyuan Xue,
Lei Lei Liu,
Chen Chen Liu,
Zhang Yue Cong
Publication year - 2015
Publication title -
food and nutrition research/food and nutrition research. supplement
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 37
eISSN - 1654-6628
pISSN - 1654-661X
DOI - 10.3402/fnr.v59.28879
Subject(s) - histopathology , medicine , copd , lung , h&e stain , immunohistochemistry , pathology , toxicity , tumor necrosis factor alpha , prednisolone , pharmacology
Highlights : (1) Potato extract (PE) exhibits non-toxic effects on mice. (2) Cigarette smoke (CS)–induced COPD rats exhibit significant thickened and disordered lung markings. (3) PE could improve the histopathological symptoms of lung tissue in COPD. (4) PE could increase the expression of IL-10 and reduce the expression of TNF-α and G-CSF in COPD rats. Objective This study aimed to evaluate the therapeutic effects of potato extract (PE) on cigarette smoke (CS)–induced chronic obstructive pulmonary disease (COPD). Methods PE was first prepared by frozen centrifugation, and its amino acid composition was detected. Toxicity of PE was analyzed by changes in morphology, behavior, routine blood indexes, and biochemical criteria of mice. Then, the COPD rat model was established by CS exposure, and PE, doxofylline, and prednisolone acetate were used to treat these rats. After 45 days of treatment, the morphology and behavior of rats were recorded. In addition, the histopathology of lung tissue was evaluated by chest x-ray and hematoxylin and eosin staining. The expression of interleukine-10 (IL-10), tumor necrosis factor-α (TNF-α), and granulocyte colony-stimulating factor (G-CSF) was detected in serum and lung tissue by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. Results Various amino acids were identified in PE, and no toxicity was exhibited in mice. The CS-induced COPD rat model was successfully established, which exhibited significant thickened and disordered lung markings on 90% of the rats. After administering doxofylline and prednisolone acetate, inflammation symptoms were improved. However, side effects such as emaciation, weakness, and loosening of teeth appeared. In the PE group, obviously improved histopathology was observed in lung tissues. Meanwhile, it was revealed that PE could increase the expression of IL-10 and reduce the expression of TNF-α and G-CSF in COPD rats, and doxofylline and prednisolone acetate also elicited similar results. Conclusion Our study suggests PE might be effective in the treatment of CS-induced COPD by inhibiting inflammation.