4.6 Article

Establishment and Evaluation of a Rat Model of Sidestream Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

Journal

FRONTIERS IN PHYSIOLOGY
Volume 9, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2018.00058

Keywords

chronic obstructive pulmonary disease; passives moking; cigarette smoke; rat model; airway remodeling

Categories

Funding

  1. National Natural Science Foundation of China (Beijing, China) [81573758, 81302931, 81760810, 8150150396]
  2. Development Project of Shanghai Peak Disciplines-Integrative Medicine [20150407]
  3. Jiangxi Provincial Plan Projects of Science and Technology, China [20151BBG70075, 20171BAB205086]
  4. Jiangxi Provincial Project of Science and Technology of TCM [2015A241]
  5. Research Projects on the Study of Integrated Traditional Chinese Medicine and Western Medicine, Xinjiang Uyghur Autonomous Region, China [2017-03-11]
  6. National Natural Science Foundation for Distinguished Young Scholars of China [81403148]
  7. Science and Technology Innovation Projects of Traditional Chinese Medicine of Shanghai Municipal Commission of Health and Family Planning, China [ZYKC201602001]

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Chronic obstructive pulmonary disease (COPD) is a common cause of mortality worldwide. The current lack of an animal model that can be established within a certain time frame and imitate the unique features of the disease is a major limiting factor in its study. The present study established and evaluated an animal model of COPD that represents the early and advanced stage features using short-, middle-, and long-term sidestream cigarette smoke (CS) exposure. One hundred and nine Sprague-Dawley rats were randomly divided into 10 groups for different periods of sidestream CS exposure or no exposure (i.e., normal groups). The rats were exposed to CS from 3R4F cigarettes in an exposure chamber. Histological analysis was performed to determine pathological changes. We also conducted open-field tests, lung function evaluations, and cytokine analysis of the blood serum, bronchoalveolar lavage fluid, and lung tissue. The lung tissue protein levels, blood gases, and were also analyzed. As the CS exposure time increased, the indicators associated with oxidative stress, inflammatory responses, and airway remodeling were greater in the CS exposure groups than in the normal group. At 24 and 36 weeks, the COPD model rats displayed the middle-and advanced-stage features of COPD, respectively. In the 8-week CS exposure group, after the CS exposure was stopped for 4 weeks, inflammatory responses and oxidative responses were ameliorated and lung function exacerbation was reduced compared with the 12-week CS exposure group. Therefore, we established a more adequate rat model of sidestream CS induced COPD, which will have great significance for a better understanding of the pathogenesis of COPD and drug effectiveness evaluation.

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