4.7 Article

Metabolic changes of H2S in smokers and patients of COPD which might involve in inflammation, oxidative stress and steroid sensitivity

Journal

SCIENTIFIC REPORTS
Volume 5, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/srep14971

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Funding

  1. National Nature Science Foundation of China [81170012, 81370141]
  2. Research Special Fund for Public Welfare Industry of Health [201002008]
  3. Capital Medicine Development Fund [2011-1004-01]

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Oxidative stress and inflammation play crucial role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Most patients with COPD show a poor response to corticosteroids. Hydrogen sulfide (H2S) has been implicated in the pathogenesis of COPD, but its expression and effects in lung tissue from COPD patients are not clear. In peripheral lung tissue samples from 24 patients, we found that compared with nonsmokers, the protein level of cystathionine-gamma-lyase (CSE) was decreased in smokers and COPD patients. CSE mRNA increased but cystathionine-beta-synthase (CBS) mRNA decreased in COPD patients. H2S donors increased glutathione and superoxide dismutase in CS exposed U937 cells and inhibited CS-induced TNF-alpha and IL-8 secretion. Dexamethasone alone had no effect on lipopolysaccharide (LPS) induced TNF-alpha release by alveolar macrophages from CS exposed rats, however the combination of dexamethasone and H2S donor significantly inhibited TNF-alpha release. Thus, H2S metabolism is altered in lung tissue of smokers and COPD patients. Supplementation of H2S protects against CS-induced oxidative stress and inflammation in macrophages and H2S on steroid sensitivity deserves further investigation.

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