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Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis

Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known...

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Autores principales: Fusco, Roberta, Cordaro, Marika, Genovese, Tiziana, Impellizzeri, Daniela, Siracusa, Rosalba, Gugliandolo, Enrico, Peritore, Alessio Filippo, D’Amico, Ramona, Crupi, Rosalia, Cuzzocrea, Salvatore, Di Paola, Rosanna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402091/
https://www.ncbi.nlm.nih.gov/pubmed/32660140
http://dx.doi.org/10.3390/antiox9070601
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author Fusco, Roberta
Cordaro, Marika
Genovese, Tiziana
Impellizzeri, Daniela
Siracusa, Rosalba
Gugliandolo, Enrico
Peritore, Alessio Filippo
D’Amico, Ramona
Crupi, Rosalia
Cuzzocrea, Salvatore
Di Paola, Rosanna
author_facet Fusco, Roberta
Cordaro, Marika
Genovese, Tiziana
Impellizzeri, Daniela
Siracusa, Rosalba
Gugliandolo, Enrico
Peritore, Alessio Filippo
D’Amico, Ramona
Crupi, Rosalia
Cuzzocrea, Salvatore
Di Paola, Rosanna
author_sort Fusco, Roberta
collection PubMed
description Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known anti-inflammatory and anti-oxidant compound. In this study, we investigated the efficacy of adelmidrol (10 mg/Kg) for bleomycin-induced pulmonary fibrosis in mice. Methods: Bleomycin intratracheal administration was performed on the first day and for the following twenty-one days, mice were treated with adelmidrol (10 mg/Kg). Results: The survival rate and body weight gain were recorded daily. At the end of the experiment, adelmidrol-administered animals showed reduced airway infiltration by inflammatory cells, Myeloperoxidase (MPO) activity, and pro-inflammatory cytokine overexpression (IL,6 IL-1β, TNF-α, and TGF-1β). Moreover, adelmidrol treatment was able to manage the significant incapacity of antioxidants and elevation of the oxidant burden, as shown by the MDA, SOD, and GSH levels and decreased nitric oxide production. It was also able to significantly modulate the JAK2/STAT3 and IκBα/NF-kB pathway. Histologic examination of the lung tissues showed reduced sample injury, mast cell degranulation, chymase activity, and collagen deposition. Conclusions: In sum, our results propose adelmidrol as a therapeutic approach in the treatment of pulmonary fibrosis.
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spelling pubmed-74020912020-08-07 Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis Fusco, Roberta Cordaro, Marika Genovese, Tiziana Impellizzeri, Daniela Siracusa, Rosalba Gugliandolo, Enrico Peritore, Alessio Filippo D’Amico, Ramona Crupi, Rosalia Cuzzocrea, Salvatore Di Paola, Rosanna Antioxidants (Basel) Article Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known anti-inflammatory and anti-oxidant compound. In this study, we investigated the efficacy of adelmidrol (10 mg/Kg) for bleomycin-induced pulmonary fibrosis in mice. Methods: Bleomycin intratracheal administration was performed on the first day and for the following twenty-one days, mice were treated with adelmidrol (10 mg/Kg). Results: The survival rate and body weight gain were recorded daily. At the end of the experiment, adelmidrol-administered animals showed reduced airway infiltration by inflammatory cells, Myeloperoxidase (MPO) activity, and pro-inflammatory cytokine overexpression (IL,6 IL-1β, TNF-α, and TGF-1β). Moreover, adelmidrol treatment was able to manage the significant incapacity of antioxidants and elevation of the oxidant burden, as shown by the MDA, SOD, and GSH levels and decreased nitric oxide production. It was also able to significantly modulate the JAK2/STAT3 and IκBα/NF-kB pathway. Histologic examination of the lung tissues showed reduced sample injury, mast cell degranulation, chymase activity, and collagen deposition. Conclusions: In sum, our results propose adelmidrol as a therapeutic approach in the treatment of pulmonary fibrosis. MDPI 2020-07-09 /pmc/articles/PMC7402091/ /pubmed/32660140 http://dx.doi.org/10.3390/antiox9070601 Text en © 2020 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Fusco, Roberta
Cordaro, Marika
Genovese, Tiziana
Impellizzeri, Daniela
Siracusa, Rosalba
Gugliandolo, Enrico
Peritore, Alessio Filippo
D’Amico, Ramona
Crupi, Rosalia
Cuzzocrea, Salvatore
Di Paola, Rosanna
Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title_full Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title_fullStr Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title_full_unstemmed Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title_short Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
title_sort adelmidrol: a new promising antioxidant and anti-inflammatory therapeutic tool in pulmonary fibrosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402091/
https://www.ncbi.nlm.nih.gov/pubmed/32660140
http://dx.doi.org/10.3390/antiox9070601
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