Tags

Type your tag names separated by a space and hit enter

Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness.
Am J Respir Cell Mol Biol 2015; 52(1):129-37AJ

Abstract

Exposure to ozone has been associated with airway inflammation, oxidative stress, and bronchial hyperresponsiveness. The goal of this study was to examine whether these adverse effects of ozone could be prevented or reversed by hydrogen sulfide (H2S) as a reducing agent. The H2S donor sodium (NaHS) (2 mg/kg) or vehicle (PBS) was intraperitoneally injected into mice 1 hour before and after 3-hour ozone (2.5 ppm) or air exposure, and the mice were studied 24 hours later. Preventive and therapeutic treatment with NaHS reduced the ozone-induced increases in the total cells, including neutrophils and macrophages; this treatment also reduced levels of cytokines, including TNF-α, chemokine (C-X-C motif) ligand 1, IL-6, and IL-1β levels in bronchial alveolar lavage fluid; inhibited bronchial hyperresponsiveness; and attenuated ozone-induced increases in total malondialdehyde in bronchoalveolar lavage fluid and decreases in the ratio of reduced glutathione/oxidized glutathione in the lung. Ozone exposure led to decreases in the H2S production rate and in mRNA and protein levels of cystathionine-β-synthetase and cystathionine-γ-lyase in the lung. These effects were prevented and reversed by NaHS treatment. Furthermore, NaHS prevented and reversed the phosphorylation of p38 mitogen-activated protein kinase and heat shock protein 27. H2S may have preventive and therapeutic value in the treatment of airway diseases that have an oxidative stress basis.

Authors+Show Affiliations

1 Department of Respiratory Medicine, and.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25010831

Citation

Zhang, Pengyu, et al. "Inhibitory Effect of Hydrogen Sulfide On Ozone-induced Airway Inflammation, Oxidative Stress, and Bronchial Hyperresponsiveness." American Journal of Respiratory Cell and Molecular Biology, vol. 52, no. 1, 2015, pp. 129-37.
Zhang P, Li F, Wiegman CH, et al. Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness. Am J Respir Cell Mol Biol. 2015;52(1):129-37.
Zhang, P., Li, F., Wiegman, C. H., Zhang, M., Hong, Y., Gong, J., ... Zhou, X. (2015). Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness. American Journal of Respiratory Cell and Molecular Biology, 52(1), pp. 129-37. doi:10.1165/rcmb.2013-0415OC.
Zhang P, et al. Inhibitory Effect of Hydrogen Sulfide On Ozone-induced Airway Inflammation, Oxidative Stress, and Bronchial Hyperresponsiveness. Am J Respir Cell Mol Biol. 2015;52(1):129-37. PubMed PMID: 25010831.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness. AU - Zhang,Pengyu, AU - Li,Feng, AU - Wiegman,Coen H, AU - Zhang,Min, AU - Hong,Yan, AU - Gong,Jicheng, AU - Chang,Yan, AU - Zhang,Junfeng Jim, AU - Adcock,Ian, AU - Chung,Kian Fan, AU - Zhou,Xin, PY - 2014/7/11/entrez PY - 2014/7/11/pubmed PY - 2015/3/12/medline KW - airway inflammation KW - bronchial hyperresponsiveness KW - hydrogen sulfide KW - oxidative stress KW - ozone SP - 129 EP - 37 JF - American journal of respiratory cell and molecular biology JO - Am. J. Respir. Cell Mol. Biol. VL - 52 IS - 1 N2 - Exposure to ozone has been associated with airway inflammation, oxidative stress, and bronchial hyperresponsiveness. The goal of this study was to examine whether these adverse effects of ozone could be prevented or reversed by hydrogen sulfide (H2S) as a reducing agent. The H2S donor sodium (NaHS) (2 mg/kg) or vehicle (PBS) was intraperitoneally injected into mice 1 hour before and after 3-hour ozone (2.5 ppm) or air exposure, and the mice were studied 24 hours later. Preventive and therapeutic treatment with NaHS reduced the ozone-induced increases in the total cells, including neutrophils and macrophages; this treatment also reduced levels of cytokines, including TNF-α, chemokine (C-X-C motif) ligand 1, IL-6, and IL-1β levels in bronchial alveolar lavage fluid; inhibited bronchial hyperresponsiveness; and attenuated ozone-induced increases in total malondialdehyde in bronchoalveolar lavage fluid and decreases in the ratio of reduced glutathione/oxidized glutathione in the lung. Ozone exposure led to decreases in the H2S production rate and in mRNA and protein levels of cystathionine-β-synthetase and cystathionine-γ-lyase in the lung. These effects were prevented and reversed by NaHS treatment. Furthermore, NaHS prevented and reversed the phosphorylation of p38 mitogen-activated protein kinase and heat shock protein 27. H2S may have preventive and therapeutic value in the treatment of airway diseases that have an oxidative stress basis. SN - 1535-4989 UR - https://www.unboundmedicine.com/medline/citation/25010831/Inhibitory_effect_of_hydrogen_sulfide_on_ozone_induced_airway_inflammation_oxidative_stress_and_bronchial_hyperresponsiveness_ L2 - http://www.atsjournals.org/doi/full/10.1165/rcmb.2013-0415OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -