title: Metabolic changes of H2S in smokers and patients of COPD which might involve in inflammation, oxidative stress and steroid sensitivity.
abstract: 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-γ-lyase (CSE) was decreased in smokers and COPD patients. CSE mRNA increased but cystathionine-β-synthase (CBS) mRNA decreased in COPD patients. H2S donors increased glutathione and superoxide dismutase in CS exposed U937 cells and inhibited CS-induced TNF-α and IL-8 secretion. Dexamethasone alone had no effect on lipopolysaccharide (LPS) induced TNF-α release by alveolar macrophages from CS exposed rats, however the combination of dexamethasone and H2S donor significantly inhibited TNF-α 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.
authors.affiliation: Pulmonary and Critical Care Medicine Department, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Department of Thoracic Surgery, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Keyi
authors.initials: K
authors.lastname: Wang
authors.affiliation: Pulmonary and Critical Care Medicine Department, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Min-Xia
authors.initials: MX
authors.lastname: Li
authors.affiliation: Department of Thoracic Surgery, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Wei
authors.initials: W
authors.lastname: He
authors.affiliation: Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing 100191, China.
authors.forename: Jin-Rui
authors.initials: JR
authors.lastname: Chang
authors.affiliation: Pulmonary and Critical Care Medicine Department, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Cheng-Cheng
authors.initials: CC
authors.lastname: Liao
authors.affiliation: Pulmonary and Critical Care Medicine Department, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Lin
authors.affiliation: Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing 100191, China.
authors.forename: Yong-Fen
authors.initials: YF
authors.lastname: Qi
authors.affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
authors.affiliation: Pulmonary and Critical Care Medicine Department, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Ya-Hong
authors.initials: YH
authors.lastname: Chen
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D045744:Cell Line, Tumor; D003541:Cystathionine beta-Synthase / Q000235:genetics / Q000378:metabolism; D003542:Cystathionine gamma-Lyase / Q000235:genetics / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D005786:Gene Expression Regulation; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism / Q000494:pharmacology; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D012907:Smoking / Q000009:adverse effects; D013440:Sulfides / Q000378:metabolism / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000305:Adrenal Cortex Hormones; D000893:Anti-Inflammatory Agents; D016209:Interleukin-8; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D013482:Superoxide Dismutase; D003541:Cystathionine beta-Synthase; D003542:Cystathionine gamma-Lyase; C025451:sodium bisulfide; D005978:Glutathione; D006862:Hydrogen Sulfide