<?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%">Li, F.</style></author><author><style face="normal" font="default" size="100%">P. Zhang</style></author><author><style face="normal" font="default" size="100%">Zhang, M.</style></author><author><style face="normal" font="default" size="100%">Liang, L.</style></author><author><style face="normal" font="default" size="100%">Sun, X.</style></author><author><style face="normal" font="default" size="100%">M. Li</style></author><author><style face="normal" font="default" size="100%">Y. Tang</style></author><author><style face="normal" font="default" size="100%">Bao, A.</style></author><author><style face="normal" font="default" size="100%">Gong, J.</style></author><author><style face="normal" font="default" size="100%">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%">Hydrogen Sulfide Prevents and Partially Reverses Ozone-Induced Features of Lung Inflammation and Emphysema in Mice</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Respir Cell Mol Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am J Resp Cell MolAm J Resp Cell Mol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">*hydrogen sulfide</style></keyword><keyword><style  face="normal" font="default" size="100%">*lung inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">*ozone exposure</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomarkers/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Blotting, Western</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchi/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchoalveolar Lavage Fluid</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase 1/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase 3/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen Sulfide/pharmacology/*therapeutic use</style></keyword><keyword><style  face="normal" font="default" size="100%">Imaging, Three-Dimensional</style></keyword><keyword><style  face="normal" font="default" size="100%">Intracellular Signaling Peptides and Proteins/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidants/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Ozone/*adverse effects</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%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pneumonia/*complications/diagnostic imaging/*drug therapy/physiopathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Proto-Oncogene Proteins c-akt/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Pulmonary Emphysema/*complications/diagnostic imaging/*drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Respiratory Function Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger/genetics/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">therapy/physiopathology</style></keyword><keyword><style  face="normal" font="default" size="100%">X-Ray Microtomography</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jul</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2016/01/06</style></edition><volume><style face="normal" font="default" size="100%">55</style></volume><pages><style face="normal" font="default" size="100%">72-81</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%">Hydrogen sulfide (H2S), a novel signaling gasotransmitter in the respiratory system, may have antiinflammatory properties in the lung. We examined the preventive and therapeutic effects of H2S on ozone-induced features of lung inflammation and emphysema. C57/BL6 mice were exposed to ozone or filtered air over 6 weeks. Sodium hydrogen sulfide (NaHS), an H2S donor, was administered to the mice either before ozone exposure (preventive effect) or after completion of 6 weeks of ozone exposure (therapeutic effect). The ozone-exposed mice developed emphysema, measured by micro-computed tomography and histology, airflow limitation, measured by the forced maneuver system, and increased lung inflammation with augmented IL-1beta, IL-18, and matrix metalloproteinase-9 (MMP-9) gene expression. Ozone-induced changes were associated with increased Nod-like receptor pyrin domain containing 3 (NLRP3)-caspase-1 activation and p38 mitogen-activated protein kinase phosphorylation and decreased Akt phosphorylation. NaHS both prevented and reversed lung inflammation and emphysematous changes in alveolar space. In contrast, NaHS prevented, but did not reverse, ozone-induced airflow limitation and bronchial structural remodeling. In conclusion, NaHS administration prevented and partially reversed ozone-induced features of lung inflammation and emphysema via regulation of the NLRP3-caspase-1, p38 mitogen-activated protein kinase, and Akt pathways.</style></abstract><accession-num><style face="normal" font="default" size="100%">26731380</style></accession-num><notes><style face="normal" font="default" size="100%">Li, FengZhang, PengyuZhang, MinLiang, LiSun, XiaoyuanLi, MinTang, YueqinBao, AihuaGong, JichengZhang, JunfengAdcock, IanChung, Kian FanZhou, XinengResearch Support, Non-U.S. Gov'tAm J Respir Cell Mol Biol. 2016 Jul;55(1):72-81. doi: 10.1165/rcmb.2015-0014OC.</style></notes><auth-address><style face="normal" font="default" size="100%">1 Department of Respiratory Medicine and.2 Department of Respiratory Medicine, Shanghai Third People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.3 Experimental Research Center, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai, People's Republic of China.4 Division of Environmental Sciences and Policy, Nicholas School of the Environment and Duke Global Health Institute, Duke University, Durham, North Carolina; and.5 Airway Diseases Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.</style></auth-address></record></records></xml>