<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">P. Zhang</style></author><author><style face="normal" font="default" size="100%">Li, F.</style></author><author><style face="normal" font="default" size="100%">Wiegman, C. H.</style></author><author><style face="normal" font="default" size="100%">Zhang, M.</style></author><author><style face="normal" font="default" size="100%">Hong, Y.</style></author><author><style face="normal" font="default" size="100%">Gong, J.</style></author><author><style face="normal" font="default" size="100%">Chang, Y.</style></author><author><style face="normal" font="default" size="100%">J.J. Zhang</style></author><author><style face="normal" font="default" size="100%">Adcock, I.</style></author><author><style face="normal" font="default" size="100%">Chung, K. F.</style></author><author><style face="normal" font="default" size="100%">X. Zhou</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness</style></title><secondary-title><style face="normal" font="default" size="100%">American Journal of Respiratory Cell and Molecular Biology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am J Resp Cell Mol</style></alt-title><short-title><style face="normal" font="default" size="100%">Am J Resp Cell Mol</style></short-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">airway inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchial Hyperreactivity/chemically induced/*drug therapy/metabolism/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">bronchial hyperresponsiveness</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchoalveolar Lavage</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystathionine beta-Synthase/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystathionine gamma-Lyase/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Gasotransmitters/*pharmacology</style></keyword><keyword><style  face="normal" font="default" size="100%">HSP27 Heat-Shock Proteins/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">hydrogen sulfide</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen Sulfide/*pharmacology</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation/chemically induced/metabolism/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Malondialdehyde/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidants, Photochemical/*adverse effects/pharmacology</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress/*drug effects</style></keyword><keyword><style  face="normal" font="default" size="100%">ozone</style></keyword><keyword><style  face="normal" font="default" size="100%">Ozone/*adverse effects/pharmacology</style></keyword><keyword><style  face="normal" font="default" size="100%">p38 Mitogen-Activated Protein Kinases/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger/metabolism</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2014/07/11</style></edition><volume><style face="normal" font="default" size="100%">52</style></volume><pages><style face="normal" font="default" size="100%">129-37</style></pages><isbn><style face="normal" font="default" size="100%">1535-4989 (Electronic)1044-1549 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">English</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;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-alpha, chemokine (C-X-C motif) ligand 1, IL-6, and IL-1beta 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-beta-synthetase and cystathionine-gamma-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.&lt;/p&gt;</style></abstract><accession-num><style face="normal" font="default" size="100%">25010831</style></accession-num><notes><style face="normal" font="default" size="100%">&lt;p&gt;Zhang, PengyuLi, FengWiegman, Coen HZhang, MinHong, YanGong, JichengChang, YanZhang, Junfeng JimAdcock, IanChung, Kian FanZhou, XinengResearch Support, Non-U.S. Gov'tAm J Respir Cell Mol Biol. 2015 Jan;52(1):129-37. doi: 10.1165/rcmb.2013-0415OC.&lt;/p&gt;</style></notes><auth-address><style face="normal" font="default" size="100%">1 Department of Respiratory Medicine, and.</style></auth-address></record></records></xml>