title: Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice.
abstract: The aim of this work was to test the effect of treatment with hydrogen sulfide (H2S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O2, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H2S partly restored the reduced H2S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H2S attenuated hyperoxia-induced acute lung injury marked by reduced ratio of lung weight to body weight, ratio of lung wet weight to dry weight, and cell numbers and protein content in bronchoalveolar lavage (BAL) and decreased apoptosis. Treatment with H2S markedly prolonged the survival of mice under oxygen exposure. Treatment with H2S abated hyperoxia-induced oxidative stress marked by reduced malondialdehyde and peroxynitrite formation, reduced NADPH oxidase activity, enhanced translocation of nuclear factor E2-related factor (Nrf2) into nucleus and increased activity of HO-1. Treatment with H2S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H2S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H2S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H2S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.
authors.affiliation: Department of Respiratory Disease, The Chinese PLA General Hospital, Beijing 100853, China. lihuaidong2012@hotmail.com
authors.forename: Huai-Dong
authors.initials: HD
authors.lastname: Li
authors.forename: Zhao-Rui
authors.initials: ZR
authors.lastname: Zhang
authors.forename: Qing-Xiang
authors.initials: QX
authors.lastname: Zhang
authors.forename: Zhi-Chu
authors.initials: ZC
authors.lastname: Qin
authors.forename: Deng-Ming
authors.initials: DM
authors.lastname: He
authors.forename: Jin-Song
authors.initials: JS
authors.lastname: Chen
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D000818:Animals; D006862:Hydrogen Sulfide / Q000627:therapeutic use*; D018496:Hyperoxia / Q000150:complications*; D007378:Interleukins / Q000235:genetics / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D019255:NADPH Oxidases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress; D030421:Peroxynitrous Acid / Q000378:metabolism; D054390:Receptors, CCR2 / Q000235:genetics / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D007378:Interleukins; D016328:NF-kappa B; D054390:Receptors, CCR2; D042461:Vascular Endothelial Growth Factor A; D030421:Peroxynitrous Acid; D008315:Malondialdehyde; D052247:Nitric Oxide Synthase Type II; D019255:NADPH Oxidases; D006862:Hydrogen Sulfide