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Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and devastating clinical disorders with high mortality and no specific therapy. Lipopolysaccharide (LPS) is usually used intratracheally to induce ALI in mice. The aim of this study was to examine the effects of an ult...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8197255/ https://www.ncbi.nlm.nih.gov/pubmed/34073872 http://dx.doi.org/10.3390/ijms22115533 |
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author | Peritore, Alessio Filippo D’Amico, Ramona Siracusa, Rosalba Cordaro, Marika Fusco, Roberta Gugliandolo, Enrico Genovese, Tiziana Crupi, Rosalia Di Paola, Rosanna Cuzzocrea, Salvatore Impellizzeri, Daniela |
author_facet | Peritore, Alessio Filippo D’Amico, Ramona Siracusa, Rosalba Cordaro, Marika Fusco, Roberta Gugliandolo, Enrico Genovese, Tiziana Crupi, Rosalia Di Paola, Rosanna Cuzzocrea, Salvatore Impellizzeri, Daniela |
author_sort | Peritore, Alessio Filippo |
collection | PubMed |
description | Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and devastating clinical disorders with high mortality and no specific therapy. Lipopolysaccharide (LPS) is usually used intratracheally to induce ALI in mice. The aim of this study was to examine the effects of an ultramicronized preparation of palmitoylethanolamide (um-PEA) in mice subjected to LPS-induced ALI. Histopathological analysis reveals that um-PEA reduced alteration in lung after LPS intratracheal administration. Besides, um-PEA decreased wet/dry weight ratio and myeloperoxidase, a marker of neutrophils infiltration, macrophages and total immune cells number and mast cells degranulation in lung. Moreover, um-PEA could also decrease cytokines release of interleukin (IL)-6, interleukin (IL)-1β, tumor necrosis factor (TNF)-α and interleukin (IL)-18. Furthermore, um-PEA significantly inhibited the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation in ALI, and at the same time decreased extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38/MAPK) expression, that was increased after LPS administration. Our study suggested that um-PEA contrasted LPS-induced ALI, exerting its potential role as an adjuvant anti-inflammatory therapeutic for treating lung injury, maybe also by p38/NF-κB pathway. |
format | Online Article Text |
id | pubmed-8197255 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-81972552021-06-13 Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach Peritore, Alessio Filippo D’Amico, Ramona Siracusa, Rosalba Cordaro, Marika Fusco, Roberta Gugliandolo, Enrico Genovese, Tiziana Crupi, Rosalia Di Paola, Rosanna Cuzzocrea, Salvatore Impellizzeri, Daniela Int J Mol Sci Article Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and devastating clinical disorders with high mortality and no specific therapy. Lipopolysaccharide (LPS) is usually used intratracheally to induce ALI in mice. The aim of this study was to examine the effects of an ultramicronized preparation of palmitoylethanolamide (um-PEA) in mice subjected to LPS-induced ALI. Histopathological analysis reveals that um-PEA reduced alteration in lung after LPS intratracheal administration. Besides, um-PEA decreased wet/dry weight ratio and myeloperoxidase, a marker of neutrophils infiltration, macrophages and total immune cells number and mast cells degranulation in lung. Moreover, um-PEA could also decrease cytokines release of interleukin (IL)-6, interleukin (IL)-1β, tumor necrosis factor (TNF)-α and interleukin (IL)-18. Furthermore, um-PEA significantly inhibited the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation in ALI, and at the same time decreased extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38/MAPK) expression, that was increased after LPS administration. Our study suggested that um-PEA contrasted LPS-induced ALI, exerting its potential role as an adjuvant anti-inflammatory therapeutic for treating lung injury, maybe also by p38/NF-κB pathway. MDPI 2021-05-24 /pmc/articles/PMC8197255/ /pubmed/34073872 http://dx.doi.org/10.3390/ijms22115533 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Peritore, Alessio Filippo D’Amico, Ramona Siracusa, Rosalba Cordaro, Marika Fusco, Roberta Gugliandolo, Enrico Genovese, Tiziana Crupi, Rosalia Di Paola, Rosanna Cuzzocrea, Salvatore Impellizzeri, Daniela Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title | Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title_full | Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title_fullStr | Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title_full_unstemmed | Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title_short | Management of Acute Lung Injury: Palmitoylethanolamide as a New Approach |
title_sort | management of acute lung injury: palmitoylethanolamide as a new approach |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8197255/ https://www.ncbi.nlm.nih.gov/pubmed/34073872 http://dx.doi.org/10.3390/ijms22115533 |
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