Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats

Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the con...
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Autor*in:	Zhao, Yan-Rui [verfasserIn] Lv, Wen-Rui [verfasserIn] Zhou, Jun-Lin [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Carbonyl sulfide Acute lung injury Ischemia/reperfusion

Übergeordnetes Werk:	Enthalten in: European journal of medical research - London : BioMed Central, 2000, 22(2017), 1 vom: 28. März
Übergeordnetes Werk:	volume:22 ; year:2017 ; number:1 ; day:28 ; month:03

Links:	Volltext

DOI / URN:	10.1186/s40001-017-0255-z

Katalog-ID:	SPR032597487

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520			\|a Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.
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allfields	10.1186/s40001-017-0255-z doi (DE-627)SPR032597487 (SPR)s40001-017-0255-z-e DE-627 ger DE-627 rakwb eng 610 ASE Zhao, Yan-Rui verfasserin aut Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins. Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213 Lv, Wen-Rui verfasserin aut Zhou, Jun-Lin verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 22(2017), 1 vom: 28. März (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:22 year:2017 number:1 day:28 month:03 https://dx.doi.org/10.1186/s40001-017-0255-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2017 1 28 03
spelling	10.1186/s40001-017-0255-z doi (DE-627)SPR032597487 (SPR)s40001-017-0255-z-e DE-627 ger DE-627 rakwb eng 610 ASE Zhao, Yan-Rui verfasserin aut Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins. Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213 Lv, Wen-Rui verfasserin aut Zhou, Jun-Lin verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 22(2017), 1 vom: 28. März (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:22 year:2017 number:1 day:28 month:03 https://dx.doi.org/10.1186/s40001-017-0255-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2017 1 28 03
allfields_unstemmed	10.1186/s40001-017-0255-z doi (DE-627)SPR032597487 (SPR)s40001-017-0255-z-e DE-627 ger DE-627 rakwb eng 610 ASE Zhao, Yan-Rui verfasserin aut Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins. Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213 Lv, Wen-Rui verfasserin aut Zhou, Jun-Lin verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 22(2017), 1 vom: 28. März (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:22 year:2017 number:1 day:28 month:03 https://dx.doi.org/10.1186/s40001-017-0255-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2017 1 28 03
allfieldsGer	10.1186/s40001-017-0255-z doi (DE-627)SPR032597487 (SPR)s40001-017-0255-z-e DE-627 ger DE-627 rakwb eng 610 ASE Zhao, Yan-Rui verfasserin aut Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins. Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213 Lv, Wen-Rui verfasserin aut Zhou, Jun-Lin verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 22(2017), 1 vom: 28. März (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:22 year:2017 number:1 day:28 month:03 https://dx.doi.org/10.1186/s40001-017-0255-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2017 1 28 03
allfieldsSound	10.1186/s40001-017-0255-z doi (DE-627)SPR032597487 (SPR)s40001-017-0255-z-e DE-627 ger DE-627 rakwb eng 610 ASE Zhao, Yan-Rui verfasserin aut Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins. Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213 Lv, Wen-Rui verfasserin aut Zhou, Jun-Lin verfasserin aut Enthalten in European journal of medical research London : BioMed Central, 2000 22(2017), 1 vom: 28. März (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:22 year:2017 number:1 day:28 month:03 https://dx.doi.org/10.1186/s40001-017-0255-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2017 1 28 03
language	English
source	Enthalten in European journal of medical research 22(2017), 1 vom: 28. März volume:22 year:2017 number:1 day:28 month:03
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topic_facet	Carbonyl sulfide Acute lung injury Ischemia/reperfusion
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container_title	European journal of medical research
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Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Carbonyl sulfide</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Acute lung injury</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Ischemia/reperfusion</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lv, Wen-Rui</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhou, Jun-Lin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">European journal of medical research</subfield><subfield code="d">London : BioMed Central, 2000</subfield><subfield code="g">22(2017), 1 vom: 28. 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author	Zhao, Yan-Rui
spellingShingle	Zhao, Yan-Rui ddc 610 misc Carbonyl sulfide misc Acute lung injury misc Ischemia/reperfusion Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
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topic_title	610 ASE Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats Carbonyl sulfide (dpeaa)DE-He213 Acute lung injury (dpeaa)DE-He213 Ischemia/reperfusion (dpeaa)DE-He213
topic	ddc 610 misc Carbonyl sulfide misc Acute lung injury misc Ischemia/reperfusion
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title	Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
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title_full	Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
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title_sort	role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
title_auth	Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
abstract	Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.
abstractGer	Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.
abstract_unstemmed	Objective To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. Methods ALI was induced by bilateral hind limb I/R in Sprague–Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lβ, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. Results Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. Conclusion Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.
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title_short	Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats
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Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats

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