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The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice
BACKGROUND: Acute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928852/ https://www.ncbi.nlm.nih.gov/pubmed/29677174 http://dx.doi.org/10.12659/MSM.906016 |
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author | Gao, Ye Wang, Ni Li, Rui H. Xiao, Yang Z. |
author_facet | Gao, Ye Wang, Ni Li, Rui H. Xiao, Yang Z. |
author_sort | Gao, Ye |
collection | PubMed |
description | BACKGROUND: Acute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship between autophagy and CXCL16 in ALI is still unclear. This study aimed to investigate the role of autophagy and chemokine CXCL16 in ALI in mice. MATERIAL/METHODS: Thirty-two male C57BL/6 mice were divided into four groups. The control group (C group) was given normal saline through intraperitoneal injection. The L group was given LPS (lipopolysaccharide) at 30 mg/kg to construct an ALI model. The 3-MA group received an intraperitoneal injection of inhibitor of autophagy 3-methyladenine at 15 mg/kg, 30 minutes before LPS injection. The anti-CXCL16 group was given 20 mg/kg of CXCL16 monoclonal antibody 30 minutes before the LPS injection. RESULTS: In the 3-MA Group, the level of histological analysis, lung wet/dry ratio, total protein of BAL (bronchoalveolar lavage fluid) and TNF-α level were higher than the L group (p<0.05), the level of autophagy was lower than the L group (p<0.05), and the level of CXCL16 was higher than the L group (p<0.05). In the anti-CXCL16 group, the level of histological analysis, lung wet/dry ratio, BAL protein, and TNF-α level were declined compared to the L group (p<0.05), but there was no statistically significant difference in expression of CXCL16 detected by ELISA between the anti-CXCL16 group and the L group (p>0.05). CONCLUSIONS: Autophagy played a protective role in ALI induced by LPS in mice. Autophagy could regulate the level of CXCL16. The chemokine CXCL16 could exacerbate ALI. |
format | Online Article Text |
id | pubmed-5928852 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-59288522018-05-01 The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice Gao, Ye Wang, Ni Li, Rui H. Xiao, Yang Z. Med Sci Monit Animal Study BACKGROUND: Acute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship between autophagy and CXCL16 in ALI is still unclear. This study aimed to investigate the role of autophagy and chemokine CXCL16 in ALI in mice. MATERIAL/METHODS: Thirty-two male C57BL/6 mice were divided into four groups. The control group (C group) was given normal saline through intraperitoneal injection. The L group was given LPS (lipopolysaccharide) at 30 mg/kg to construct an ALI model. The 3-MA group received an intraperitoneal injection of inhibitor of autophagy 3-methyladenine at 15 mg/kg, 30 minutes before LPS injection. The anti-CXCL16 group was given 20 mg/kg of CXCL16 monoclonal antibody 30 minutes before the LPS injection. RESULTS: In the 3-MA Group, the level of histological analysis, lung wet/dry ratio, total protein of BAL (bronchoalveolar lavage fluid) and TNF-α level were higher than the L group (p<0.05), the level of autophagy was lower than the L group (p<0.05), and the level of CXCL16 was higher than the L group (p<0.05). In the anti-CXCL16 group, the level of histological analysis, lung wet/dry ratio, BAL protein, and TNF-α level were declined compared to the L group (p<0.05), but there was no statistically significant difference in expression of CXCL16 detected by ELISA between the anti-CXCL16 group and the L group (p>0.05). CONCLUSIONS: Autophagy played a protective role in ALI induced by LPS in mice. Autophagy could regulate the level of CXCL16. The chemokine CXCL16 could exacerbate ALI. International Scientific Literature, Inc. 2018-04-20 /pmc/articles/PMC5928852/ /pubmed/29677174 http://dx.doi.org/10.12659/MSM.906016 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Animal Study Gao, Ye Wang, Ni Li, Rui H. Xiao, Yang Z. The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title | The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title_full | The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title_fullStr | The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title_full_unstemmed | The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title_short | The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice |
title_sort | role of autophagy and the chemokine (c-x-c motif) ligand 16 during acute lung injury in mice |
topic | Animal Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928852/ https://www.ncbi.nlm.nih.gov/pubmed/29677174 http://dx.doi.org/10.12659/MSM.906016 |
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