Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice
The aim of this work was to test the effect of treatment with hydrogen sulfide (H 2 S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O 2 , and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H 2 S partly restor...
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| Veröffentlicht in: | European journal of applied physiology 2013-06, Vol.113 (6), p.1555-1563 |
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| creator | Li, Huai-Dong Zhang, Zhao-Rui Zhang, Qing-Xiang Qin, Zhi-Chu He, Deng-Ming Chen, Jin-Song |
| description | The aim of this work was to test the effect of treatment with hydrogen sulfide (H
2
S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O
2
, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H
2
S partly restored the reduced H
2
S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H
2
S 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 H
2
S markedly prolonged the survival of mice under oxygen exposure. Treatment with H
2
S 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 H
2
S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H
2
S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H
2
S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H
2
S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice. |
| doi_str_mv | 10.1007/s00421-012-2584-5 |
| format | Article |
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2
S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O
2
, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H
2
S partly restored the reduced H
2
S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H
2
S 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 H
2
S markedly prolonged the survival of mice under oxygen exposure. Treatment with H
2
S 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 H
2
S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H
2
S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H
2
S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H
2
S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.</description><identifier>ISSN: 1439-6319</identifier><identifier>EISSN: 1439-6327</identifier><identifier>DOI: 10.1007/s00421-012-2584-5</identifier><identifier>PMID: 23307012</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Acute Lung Injury - drug therapy ; Acute Lung Injury - etiology ; Acute Lung Injury - metabolism ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Edema ; Human Physiology ; Hydrogen ; Hydrogen Sulfide - therapeutic use ; Hyperoxia ; Hyperoxia - complications ; Interleukins - genetics ; Interleukins - metabolism ; Lavage ; Lungs ; Malondialdehyde - metabolism ; Mice ; Mice, Inbred C57BL ; NADPH Oxidases - metabolism ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Occupational Medicine/Industrial Medicine ; Original Article ; Oxidative Stress ; Permeability ; Peroxynitrous Acid - metabolism ; Proteins ; Receptors, CCR2 - genetics ; Receptors, CCR2 - metabolism ; Respiratory diseases ; Sports Medicine ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>European journal of applied physiology, 2013-06, Vol.113 (6), p.1555-1563</ispartof><rights>Springer-Verlag Berlin Heidelberg 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-bb91e4eb731e6c8537081a1b821724b0f32e7af9a3530e7a5a784b09c2255dcc3</citedby><cites>FETCH-LOGICAL-c372t-bb91e4eb731e6c8537081a1b821724b0f32e7af9a3530e7a5a784b09c2255dcc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00421-012-2584-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00421-012-2584-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23307012$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Huai-Dong</creatorcontrib><creatorcontrib>Zhang, Zhao-Rui</creatorcontrib><creatorcontrib>Zhang, Qing-Xiang</creatorcontrib><creatorcontrib>Qin, Zhi-Chu</creatorcontrib><creatorcontrib>He, Deng-Ming</creatorcontrib><creatorcontrib>Chen, Jin-Song</creatorcontrib><title>Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice</title><title>European journal of applied physiology</title><addtitle>Eur J Appl Physiol</addtitle><addtitle>Eur J Appl Physiol</addtitle><description>The aim of this work was to test the effect of treatment with hydrogen sulfide (H
2
S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O
2
, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H
2
S partly restored the reduced H
2
S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H
2
S 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 H
2
S markedly prolonged the survival of mice under oxygen exposure. Treatment with H
2
S 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 H
2
S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H
2
S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H
2
S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H
2
S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.</description><subject>Acute Lung Injury - drug therapy</subject><subject>Acute Lung Injury - etiology</subject><subject>Acute Lung Injury - metabolism</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Edema</subject><subject>Human Physiology</subject><subject>Hydrogen</subject><subject>Hydrogen Sulfide - therapeutic use</subject><subject>Hyperoxia</subject><subject>Hyperoxia - complications</subject><subject>Interleukins - genetics</subject><subject>Interleukins - metabolism</subject><subject>Lavage</subject><subject>Lungs</subject><subject>Malondialdehyde - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NADPH Oxidases - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>Permeability</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Proteins</subject><subject>Receptors, CCR2 - genetics</subject><subject>Receptors, CCR2 - metabolism</subject><subject>Respiratory diseases</subject><subject>Sports Medicine</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1439-6319</issn><issn>1439-6327</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kEtPwzAQhC0EoqXwA7ggS5wDfsR1ckQVL6kSl3I2jrNpU7VO8UO0_x5HgYoLpx15Z2atD6FrSu4oIfLeE5IzmhHKMiaKPBMnaExzXmZTzuTpUdNyhC68XxNCCkaLczRinBOZYmP0sXCgwxZswF9tWGHYd0uwXfR4dahdr7GPm6atAesQwEYdoN_twHX7VmetraOBGmsTA-BNtEvc2nV0hzTwtjVwic4avfFw9TMn6P3pcTF7yeZvz6-zh3lmuGQhq6qSQg6V5BSmphBckoJqWqUPS5ZXpOEMpG5KzQUnSQkti_RcGsaEqI3hE3Q79O5c9xnBB7XuorPppKI5ZbmgMkUniA4u4zrvHTRq59qtdgdFieqZqoGpSnBUz1T1mZuf5lhtoT4mfiEmAxsMPq3sEtyf0_-2fgOFAIJk</recordid><startdate>20130601</startdate><enddate>20130601</enddate><creator>Li, Huai-Dong</creator><creator>Zhang, Zhao-Rui</creator><creator>Zhang, Qing-Xiang</creator><creator>Qin, Zhi-Chu</creator><creator>He, Deng-Ming</creator><creator>Chen, Jin-Song</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20130601</creationdate><title>Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice</title><author>Li, Huai-Dong ; Zhang, Zhao-Rui ; Zhang, Qing-Xiang ; Qin, Zhi-Chu ; He, Deng-Ming ; Chen, Jin-Song</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-bb91e4eb731e6c8537081a1b821724b0f32e7af9a3530e7a5a784b09c2255dcc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acute Lung Injury - drug therapy</topic><topic>Acute Lung Injury - etiology</topic><topic>Acute Lung Injury - metabolism</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Edema</topic><topic>Human Physiology</topic><topic>Hydrogen</topic><topic>Hydrogen Sulfide - therapeutic use</topic><topic>Hyperoxia</topic><topic>Hyperoxia - complications</topic><topic>Interleukins - genetics</topic><topic>Interleukins - metabolism</topic><topic>Lavage</topic><topic>Lungs</topic><topic>Malondialdehyde - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NADPH Oxidases - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Occupational Medicine/Industrial Medicine</topic><topic>Original Article</topic><topic>Oxidative Stress</topic><topic>Permeability</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Proteins</topic><topic>Receptors, CCR2 - genetics</topic><topic>Receptors, CCR2 - metabolism</topic><topic>Respiratory diseases</topic><topic>Sports Medicine</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Huai-Dong</creatorcontrib><creatorcontrib>Zhang, Zhao-Rui</creatorcontrib><creatorcontrib>Zhang, Qing-Xiang</creatorcontrib><creatorcontrib>Qin, Zhi-Chu</creatorcontrib><creatorcontrib>He, Deng-Ming</creatorcontrib><creatorcontrib>Chen, Jin-Song</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>European journal of applied physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Huai-Dong</au><au>Zhang, Zhao-Rui</au><au>Zhang, Qing-Xiang</au><au>Qin, Zhi-Chu</au><au>He, Deng-Ming</au><au>Chen, Jin-Song</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice</atitle><jtitle>European journal of applied physiology</jtitle><stitle>Eur J Appl Physiol</stitle><addtitle>Eur J Appl Physiol</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>113</volume><issue>6</issue><spage>1555</spage><epage>1563</epage><pages>1555-1563</pages><issn>1439-6319</issn><eissn>1439-6327</eissn><abstract>The aim of this work was to test the effect of treatment with hydrogen sulfide (H
2
S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O
2
, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H
2
S partly restored the reduced H
2
S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H
2
S 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 H
2
S markedly prolonged the survival of mice under oxygen exposure. Treatment with H
2
S 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 H
2
S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H
2
S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H
2
S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H
2
S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>23307012</pmid><doi>10.1007/s00421-012-2584-5</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1439-6319 |
| ispartof | European journal of applied physiology, 2013-06, Vol.113 (6), p.1555-1563 |
| issn | 1439-6319 1439-6327 |
| language | eng |
| recordid | cdi_proquest_journals_1412451735 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Acute Lung Injury - drug therapy Acute Lung Injury - etiology Acute Lung Injury - metabolism Animals Biomedical and Life Sciences Biomedicine Edema Human Physiology Hydrogen Hydrogen Sulfide - therapeutic use Hyperoxia Hyperoxia - complications Interleukins - genetics Interleukins - metabolism Lavage Lungs Malondialdehyde - metabolism Mice Mice, Inbred C57BL NADPH Oxidases - metabolism NF-kappa B - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Occupational Medicine/Industrial Medicine Original Article Oxidative Stress Permeability Peroxynitrous Acid - metabolism Proteins Receptors, CCR2 - genetics Receptors, CCR2 - metabolism Respiratory diseases Sports Medicine Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism |
| title | Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice |
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