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N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis
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| Zeitschriftentitel: | Bioscience Reports |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Bioscience Reports, 39, 2019, 7 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Portland Press Ltd.
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| Schlagwörter: |
| author_facet |
Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi |
|---|---|
| author |
Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi |
| spellingShingle |
Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi Bioscience Reports N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis Cell Biology Molecular Biology Biochemistry Biophysics |
| author_sort |
huang, huaping |
| spelling |
Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20190681 <jats:title>Abstract</jats:title> <jats:p>Silicosis is a lethal pneumoconiosis disease characterized by chronic lung inflammation and fibrosis. The present study was to explore the effect of against crystalline silica (CS)-induced pulmonary fibrosis. A total of 138 wild-type C57BL/6J mice were divided into control and experimental groups, and killed on month 0, 1, 2, 3, 4, and 5. Different doses of N-acetylcysteine (NAC) were gavaged to the mice after CS instillation to observe the effect of NAC on CS induced pulmonary fibrosis and inflammation. The pulmonary injury was evaluated with Hematoxylin and eosin/Masson staining. Reactive oxygen species level was analyzed by DCFH-DA labeling. Commercial ELISA kits were used to determine antioxidant activity (T-AOC, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) and cytokines (TNF-α, IL-1β, IL-4, and IL-6). The expression of oxidising enzymes (NOX2, iNOS, SOD2, and XO) were detected by real time PCR. Immunohistochemistry (IHC) staining was performed to examine epithelial-mesenchymal transition-related markers. The mice treated with NAC presented markedly reduced CS-induced pulmonary injury and ameliorated CS-induced pulmonary fibrosis and inflammation. The level of malondialdehyde was reduced, while the activities of GSH-PX, SOD, and T-AOC were markedly enhanced by NAC. We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment. Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC. These encouraging findings suggest that NAC exerts pulmonary protective effects in CS-induced pulmonary fibrosis and might be considered as a promising agent for the treatment of silicosis.</jats:p> N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis Bioscience Reports |
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| title |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_unstemmed |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_full |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_fullStr |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_full_unstemmed |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_short |
N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_sort |
n-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| topic |
Cell Biology Molecular Biology Biochemistry Biophysics |
| url |
http://dx.doi.org/10.1042/bsr20190681 |
| publishDate |
2019 |
| physical |
|
| description |
<jats:title>Abstract</jats:title>
<jats:p>Silicosis is a lethal pneumoconiosis disease characterized by chronic lung inflammation and fibrosis. The present study was to explore the effect of against crystalline silica (CS)-induced pulmonary fibrosis. A total of 138 wild-type C57BL/6J mice were divided into control and experimental groups, and killed on month 0, 1, 2, 3, 4, and 5. Different doses of N-acetylcysteine (NAC) were gavaged to the mice after CS instillation to observe the effect of NAC on CS induced pulmonary fibrosis and inflammation. The pulmonary injury was evaluated with Hematoxylin and eosin/Masson staining. Reactive oxygen species level was analyzed by DCFH-DA labeling. Commercial ELISA kits were used to determine antioxidant activity (T-AOC, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) and cytokines (TNF-α, IL-1β, IL-4, and IL-6). The expression of oxidising enzymes (NOX2, iNOS, SOD2, and XO) were detected by real time PCR. Immunohistochemistry (IHC) staining was performed to examine epithelial-mesenchymal transition-related markers. The mice treated with NAC presented markedly reduced CS-induced pulmonary injury and ameliorated CS-induced pulmonary fibrosis and inflammation. The level of malondialdehyde was reduced, while the activities of GSH-PX, SOD, and T-AOC were markedly enhanced by NAC. We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment. Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC. These encouraging findings suggest that NAC exerts pulmonary protective effects in CS-induced pulmonary fibrosis and might be considered as a promising agent for the treatment of silicosis.</jats:p> |
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| author | Huang, Huaping, Chen, Mingjing, Liu, Feng, Wu, Haifeng, Wang, Jie, Chen, Jialiang, Liu, Meihua, Li, Xi |
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| description | <jats:title>Abstract</jats:title> <jats:p>Silicosis is a lethal pneumoconiosis disease characterized by chronic lung inflammation and fibrosis. The present study was to explore the effect of against crystalline silica (CS)-induced pulmonary fibrosis. A total of 138 wild-type C57BL/6J mice were divided into control and experimental groups, and killed on month 0, 1, 2, 3, 4, and 5. Different doses of N-acetylcysteine (NAC) were gavaged to the mice after CS instillation to observe the effect of NAC on CS induced pulmonary fibrosis and inflammation. The pulmonary injury was evaluated with Hematoxylin and eosin/Masson staining. Reactive oxygen species level was analyzed by DCFH-DA labeling. Commercial ELISA kits were used to determine antioxidant activity (T-AOC, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) and cytokines (TNF-α, IL-1β, IL-4, and IL-6). The expression of oxidising enzymes (NOX2, iNOS, SOD2, and XO) were detected by real time PCR. Immunohistochemistry (IHC) staining was performed to examine epithelial-mesenchymal transition-related markers. The mice treated with NAC presented markedly reduced CS-induced pulmonary injury and ameliorated CS-induced pulmonary fibrosis and inflammation. The level of malondialdehyde was reduced, while the activities of GSH-PX, SOD, and T-AOC were markedly enhanced by NAC. We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment. Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC. These encouraging findings suggest that NAC exerts pulmonary protective effects in CS-induced pulmonary fibrosis and might be considered as a promising agent for the treatment of silicosis.</jats:p> |
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| spelling | Huang, Huaping Chen, Mingjing Liu, Feng Wu, Haifeng Wang, Jie Chen, Jialiang Liu, Meihua Li, Xi 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20190681 <jats:title>Abstract</jats:title> <jats:p>Silicosis is a lethal pneumoconiosis disease characterized by chronic lung inflammation and fibrosis. The present study was to explore the effect of against crystalline silica (CS)-induced pulmonary fibrosis. A total of 138 wild-type C57BL/6J mice were divided into control and experimental groups, and killed on month 0, 1, 2, 3, 4, and 5. Different doses of N-acetylcysteine (NAC) were gavaged to the mice after CS instillation to observe the effect of NAC on CS induced pulmonary fibrosis and inflammation. The pulmonary injury was evaluated with Hematoxylin and eosin/Masson staining. Reactive oxygen species level was analyzed by DCFH-DA labeling. Commercial ELISA kits were used to determine antioxidant activity (T-AOC, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) and cytokines (TNF-α, IL-1β, IL-4, and IL-6). The expression of oxidising enzymes (NOX2, iNOS, SOD2, and XO) were detected by real time PCR. Immunohistochemistry (IHC) staining was performed to examine epithelial-mesenchymal transition-related markers. The mice treated with NAC presented markedly reduced CS-induced pulmonary injury and ameliorated CS-induced pulmonary fibrosis and inflammation. The level of malondialdehyde was reduced, while the activities of GSH-PX, SOD, and T-AOC were markedly enhanced by NAC. We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment. Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC. These encouraging findings suggest that NAC exerts pulmonary protective effects in CS-induced pulmonary fibrosis and might be considered as a promising agent for the treatment of silicosis.</jats:p> N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis Bioscience Reports |
| spellingShingle | Huang, Huaping, Chen, Mingjing, Liu, Feng, Wu, Haifeng, Wang, Jie, Chen, Jialiang, Liu, Meihua, Li, Xi, Bioscience Reports, N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis, Cell Biology, Molecular Biology, Biochemistry, Biophysics |
| title | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_full | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_fullStr | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_full_unstemmed | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_short | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_sort | n-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| title_unstemmed | N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis |
| topic | Cell Biology, Molecular Biology, Biochemistry, Biophysics |
| url | http://dx.doi.org/10.1042/bsr20190681 |