Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1
Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells an...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Dial, Katelyn [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Umfang: |
2 |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:128 ; year:2018 ; day:20 ; month:11 ; pages:102-103 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1016/j.freeradbiomed.2018.10.245 |
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| 520 | |a Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. | ||
| 520 | |a Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. | ||
| 700 | 1 | |a Patel, Vivek |4 oth | |
| 700 | 1 | |a Wu, Wenjun |4 oth | |
| 700 | 1 | |a Mantell, Lin |4 oth | |
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10.1016/j.freeradbiomed.2018.10.245 doi GBV00000000000412.pica (DE-627)ELV044616074 (ELSEVIER)S0891-5849(18)32005-7 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Dial, Katelyn verfasserin aut Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 2018transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Patel, Vivek oth Wu, Wenjun oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 https://doi.org/10.1016/j.freeradbiomed.2018.10.245 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 128 2018 20 1120 102-103 2 128.2018, S102-, (2 S.) |
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10.1016/j.freeradbiomed.2018.10.245 doi GBV00000000000412.pica (DE-627)ELV044616074 (ELSEVIER)S0891-5849(18)32005-7 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Dial, Katelyn verfasserin aut Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 2018transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Patel, Vivek oth Wu, Wenjun oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 https://doi.org/10.1016/j.freeradbiomed.2018.10.245 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 128 2018 20 1120 102-103 2 128.2018, S102-, (2 S.) |
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10.1016/j.freeradbiomed.2018.10.245 doi GBV00000000000412.pica (DE-627)ELV044616074 (ELSEVIER)S0891-5849(18)32005-7 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Dial, Katelyn verfasserin aut Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 2018transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Patel, Vivek oth Wu, Wenjun oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 https://doi.org/10.1016/j.freeradbiomed.2018.10.245 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 128 2018 20 1120 102-103 2 128.2018, S102-, (2 S.) |
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10.1016/j.freeradbiomed.2018.10.245 doi GBV00000000000412.pica (DE-627)ELV044616074 (ELSEVIER)S0891-5849(18)32005-7 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Dial, Katelyn verfasserin aut Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 2018transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Patel, Vivek oth Wu, Wenjun oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 https://doi.org/10.1016/j.freeradbiomed.2018.10.245 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 128 2018 20 1120 102-103 2 128.2018, S102-, (2 S.) |
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10.1016/j.freeradbiomed.2018.10.245 doi GBV00000000000412.pica (DE-627)ELV044616074 (ELSEVIER)S0891-5849(18)32005-7 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Dial, Katelyn verfasserin aut Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 2018transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. Patel, Vivek oth Wu, Wenjun oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 https://doi.org/10.1016/j.freeradbiomed.2018.10.245 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 128 2018 20 1120 102-103 2 128.2018, S102-, (2 S.) |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:128 year:2018 day:20 month:11 pages:102-103 extent:2 |
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New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |
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antioxidants ameliorate hyperoxia-induced lung injury by inhibition of hmgb1 |
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Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1 |
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Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. |
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Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. |
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Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI. |
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