Involvement of endogenous hydrogen sulfide in cigarette smoke-induced changes in airway responsiveness and inflammation of rat lung
Autor: | Pei-Pei Wang, Chaoshu Tang, Yan-Jing He, Xin-Mao Wang, Yahong Chen, Wan-Zhen Yao, Yong-Fen Qi |
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Rok vydání: | 2011 |
Předmět: |
Male
medicine.medical_specialty Vasodilator Agents Immunology Glycine Enzyme-Linked Immunosorbent Assay Endogeny Inflammation Sodium hydrosulfide In Vitro Techniques Sulfides Systemic inflammation Biochemistry Rats Sprague-Dawley Glibenclamide Random Allocation chemistry.chemical_compound Smoke Internal medicine Tobacco Respiratory Hypersensitivity medicine Animals Immunology and Allergy Hydrogen Sulfide Lung Molecular Biology Dose-Response Relationship Drug Tumor Necrosis Factor-alpha Interleukin-8 Cystathionine gamma-Lyase Muscle Smooth Hematology Acetylcholine Rats Trachea Dose–response relationship medicine.anatomical_structure Endocrinology chemistry Alkynes Anesthesia medicine.symptom Muscle Contraction medicine.drug |
Zdroj: | Cytokine. 53:334-341 |
ISSN: | 1043-4666 |
DOI: | 10.1016/j.cyto.2010.12.006 |
Popis: | Hydrogen sulfide (H₂S), recently considered the third endogenous gaseous transmitter, may have an important role in systemic inflammation. We investigated whether endogenous H₂S may be a crucial mediator in airway responsiveness and airway inflammation in a rat model of chronic exposure to cigarette smoke (CS). Rats randomly divided into control and CS-exposed groups were treated with or without sodium hydrosulfide (NaHS, donor of H₂S) or propargylglycine (PPG, inhibitor of cystathionine-γ-lyase [CSE], an H₂S-synthesizing enzyme) for 4-month exposure. Serum H₂S level and CSE protein expression in lung tissue were higher, by 2.04- and 2.33-fold, respectively, in CS-exposed rats than in controls (P |
Databáze: | OpenAIRE |
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