Endogenous hydrogen sulfide reduces airway inflammation and remodeling in a rat model of asthma |
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| Authors: | Ya-Hong Chen Rui Wu Bin Geng Yong-Fen Qi Pei-Pei Wang Wan-Zhen Yao Chao-Shu Tang |
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| Affiliation: | 1. Respiratory Department, Peking University Third Hospital, Beijing 100083, China;2. Department of Physiology, Health Science Center, Peking University, Beijing 100083, China;1. Department of Anesthesiology, University of Texas Medical Branch and Shriners Burns Hospital for Children, Galveston, TX, USA;2. Laboratory of Molecular Pharmacology, Department of Pharmacy, University of Patras, Patras, Greece;1. The Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA;2. Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA;3. Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA;1. Department of Biology, Lakehead University, Thunder Bay, Canada;2. Cardiovascular and Metabolic Research Unit, Lakehead University, Thunder Bay, Canada;3. Thunder Bay Regional Research Institute, Thunder Bay, Canada;4. Department of Natural Medicine & Institute of Materia Medica, Fourth Military Medical University, Xi’an, China;5. Department of Health Sciences, Lakehead University, Thunder Bay, Canada |
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| Abstract: | ![]()
Endogenous hydrogen sulfide (H2S) is hypothesized to have an important role in systemic inflammation. We investigated if endogenous H2S may be a crucial mediator in airway inflammation and airway remodeling in a rat model of asthma and if endogenous H2S may exert its anti-inflammatory effect by inhibiting inducible nitric oxide synthase (iNOS)/NO pathway. Cystathionine-γ-lyase (CSE; a H2S-synthesizing enzyme) was mainly expressed in airway and vascular smooth muscle cells in rat lung tissue. Levels of endogenous H2S was decreased in pulmonary tissue in ovalbumin (OVA)-treated rats. Exogenous administration of NaHS alleviated airway inflammation and airway remodeling: peak expiratory flow (PEF) increased, goblet cell hyperplasia and collagen deposition score decreased, with decreased total cells recovered from bronchoalveolar fluid (BALF) and influx of eosinophils and neutrophils. The H2S levels of serum and lung tissue were positively correlated with PEF and negatively correlated with the level of eosinophils and neutrophils in BALF, score of lung pathology. NaHS treatment significantly attenuated pulmonary iNOS activation in OVA-treated rats. These results suggest that the CSE/H2S pathway plays an anti-inflammatory and anti-remodeling part in asthma pathogenesis and could be a novel target in prevention and treatment of asthma. |
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