The Preventive Effect of Exercise on the Cigarette Smoke-induced Lung Injury
| Autor: | Yu-Wen Liao, 廖毓文 |
|---|---|
| Rok vydání: | 2010 |
| Druh dokumentu: | 學位論文 ; thesis |
| Popis: | 98 Cigarette smoking (CS) is the major risk factor of chronic obstructive pulmonary disease and highly associated with various lung injuries such as inflammation, mucus hypersecretion and epithelium proliferation in lung tissue. Besides, inflammation is characterized by the increase of endothelium permeability and leukocyte infiltration, which is regulated through adhesion molecules, cytokines and chemokines. Moreover, the expressions of inflammatory molecules are mediated by nuclear factor-?羠 (NF-?羠) activation. Exercise training has been known improved pulmonary function in patients with malignant lung diseases. However, the role of exercise and its underlying mechanism in CS-induced lung injury are not fully understood. In this study, we investigated the preventive effect and its mechanisms of exercise against lung injury induced by the exposure of CS in mice. C57BL/6 mice were randomly divided into 4 groups. The animals received challenges of air, CS exposure (twice a day for 30 consecutive days), rotarod treadmill training (5 days a week for 8 weeks) or rotarod treadmill training and CS exposure. Mice were exposed to CS resulted an increase in endothelium permeability and leukocytes infiltration in lung, but the elevations were reduced by exercise training. Additionally, change of the mucin 2 expressions and the extent of epithelium thickness and proliferating cell nuclear antigen (PCNA) expression were augmented in CS group, but the alterations were impaired by exercise training as well. Moreover, leukocyte infiltration in response to CS was mediated by up-regulation of adhesion molecules (intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1) and inflammatory regulators (interleukin-1?牷Bkeratinocyte-derived chemokine、monocyte chemotactic protein-1 and macrophage inflammatory protein-2), all of which were significantly alleviated by exercise training. Furthermore, the CS-induced increase in the phosphorylation of NF-?羠 at Ser311 residue was also attenuated by exercise training. In conclusion, these findings suggest that physical exercise may prevent from CS-mediated lung injury. |
| Databáze: | Networked Digital Library of Theses & Dissertations |
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