4.6 Article

Prior exercise training alleviates the lung inflammation induced by subsequent exposure to environmental cigarette smoke

期刊

ACTA PHYSIOLOGICA
卷 205, 期 4, 页码 532-540

出版社

WILEY
DOI: 10.1111/j.1748-1716.2012.02433.x

关键词

cigarette smoke; exercise; inflammation; mucin; proliferation

资金

  1. National Scientific Council [NSC-99-2320-B-010-017-MY3, NSC-98-2320-B-010-016-MY3]
  2. National Health Research Institutes [NHRI-EX100-9608SC]
  3. VGHUST Joint Research Program
  4. Tsou's Foundation [VGHUST 100-G7-4-4, VGHUST 101-G7-5-3]
  5. Yen Tjing Ling Medical Foundation [CI-99-15, CI-100-26]
  6. Ministry of Education, Aim for the Top University Plan, VGHUST Joint Research Program, Taiwan

向作者/读者索取更多资源

Aim Environmental cigarette smoke (CS) contains many compounds that are harmful to the respiratory system and lead to chronic lung inflammation and other lung diseases. Exercise training is known to confer protection against diseases with chronic inflammation by reducing inflammatory response in human or experimental animals. In this study, we investigated the preventive effect of exercise training against lung inflammation induced by environmental CS. Methods and results In this study, two groups of mice received air exposure with (the exercise group) or without (the control group) exercise training for 8 weeks and another two groups received air exposure for the first 4 weeks and CS exposure for the following 4 weeks with (the exercise+CS group) or without (the CS group) exercise training for 8 weeks. As compared with lung tissues of control and exercise groups, those of the CS group showed significantly increased bronchoalveolar-capillary permeability, inflammatory cell infiltration, epithelial thickening, expression of proliferating cell nuclear antigen, mucin 2, cytokines, chemokines, adhesion molecules and activation of NF-?B. These CS-induced pathophysiologic consequences were largely prevented in the exercise + CS group. Conclusion Collectively, prior exercise training may protect against lung inflammation induced by environmental CS in mice by attenuating the activation of NF-?B and the production of inflammatory mediators.

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