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Hydrogen coadministration slows the development of COPD-like lung disease in a cigarette smoke-induced rat model

Authors Liu X, Ma C, Wang X, Wang W, Li Z, Wang X, Wang P, Sun W, Xue B

Received 13 October 2016

Accepted for publication 28 March 2017

Published 2 May 2017 Volume 2017:12 Pages 1309—1324

DOI https://doi.org/10.2147/COPD.S124547

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr Richard Russell

Xiaoyu Liu,1,* Cuiqing Ma,2,* Xiaoyu Wang,1 Wenjing Wang,1 Zhu Li,1 Xiansheng Wang,1 Pengyu Wang,1 Wuzhuang Sun,1 Baojian Xue3

1Department of Respiratory Medicine, The First Hospital of Hebei Medical University, 2Department of Immunology, Hebei Medical University, Shijiazhuang, 3Life Science Research Center, Hebei North University, Zhangjiakou, People’s Republic of China

*These authors contributed equally to this work

Background: Chronic obstructive pulmonary disease (COPD) is a progressive pulmonary disease caused by harmful gases or particles. Recent studies have shown that 2% hydrogen or hydrogen water is effective in the treatment and prevention of a variety of diseases. This study investigated the beneficial effects and the possible mechanisms of different hydrogen concentrations on COPD.
Methods: A rat COPD model was established through smoke exposure methods, and inhalation of different concentrations of hydrogen was used as the intervention. The daily condition of rats and the weight changes were observed; lung function and right ventricular hypertrophy index were assessed. Also, white blood cells were assessed in bronchoalveolar lavage fluid. Pathologic changes in the lung tissue were analyzed using light microscopy and electron microscopy; cardiovascular structure and pulmonary arterial pressure changes in rats were observed using ultrasonography. Tumor necrosis factor alpha, interleukin (IL)-6, IL-17, IL-23, matrix metalloproteinase-12, tissue inhibitor of metalloproteinase-1, caspase-3, caspase-8 protein, and mRNA levels in the lung tissue were determined using immunohistochemistry, Western blot, and real-time polymerase chain reaction.
Results: The results showed that hydrogen inhalation significantly reduced the number of inflammatory cells in the bronchoalveolar lavage fluid, and the mRNA and protein expression levels of tumor necrosis factor alpha, IL-6, IL-17, IL-23, matrix metalloproteinase-12, caspase-3, and caspase-8, but increased the tissue inhibitor of metalloproteinase-1 expression. Furthermore, hydrogen inhalation ameliorated lung pathology, lung function, and cardiovascular function and reduced the right ventricular hypertrophy index. Inhalation of 22% and 41.6% hydrogen showed better outcome than inhalation of 2% hydrogen.
Conclusion: These results suggest that hydrogen inhalation slows the development of COPD-like lung disease in a cigarette smoke-induced rat model. Higher concentrations of hydrogen may represent a more effective way for the rat model.

Keywords: chronic obstructive pulmonary disease, hydrogen, inflammation

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