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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.
  • Peritore AF; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • D'Amico R; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Siracusa R; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Cordaro M; Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98122 Messina, Italy.
  • Fusco R; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Gugliandolo E; Department of Veterinary Science, University of Messina, 98122 Messina, Italy.
  • Genovese T; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Crupi R; Department of Veterinary Science, University of Messina, 98122 Messina, Italy.
  • Di Paola R; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Cuzzocrea S; Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy.
  • Impellizzeri D; Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, MO 63104, USA.
Int J Mol Sci ; 22(11)2021 May 24.
Article in English | MEDLINE | ID: covidwho-1273453
Semantic information from SemMedBD (by NLM)
1. Lipopolysaccharides CAUSES Acute Lung Injury
Subject
Lipopolysaccharides
Predicate
CAUSES
Object
Acute Lung Injury
2. Mus LOCATION_OF palmidrol
Subject
Mus
Predicate
LOCATION_OF
Object
palmidrol
3. Peas - dietary PREDISPOSES Acute inflammation
Subject
Peas - dietary
Predicate
PREDISPOSES
Object
Acute inflammation
4. cytokine PRODUCES interleukin-6
Subject
cytokine
Predicate
PRODUCES
Object
interleukin-6
5. Inhibitor PART_OF B-Lymphocytes
Subject
Inhibitor
Predicate
PART_OF
Object
B-Lymphocytes
6. Polypeptides COEXISTS_WITH Inhibitor
Subject
Polypeptides
Predicate
COEXISTS_WITH
Object
Inhibitor
7. Polypeptides STIMULATES B-Lymphocytes
Subject
Polypeptides
Predicate
STIMULATES
Object
B-Lymphocytes
8. Polypeptides ASSOCIATED_WITH Acute Lung Injury
Subject
Polypeptides
Predicate
ASSOCIATED_WITH
Object
Acute Lung Injury
9. Lipopolysaccharides CAUSES Acute Lung Injury
Subject
Lipopolysaccharides
Predicate
CAUSES
Object
Acute Lung Injury
10. Mus LOCATION_OF palmidrol
Subject
Mus
Predicate
LOCATION_OF
Object
palmidrol
11. Peas - dietary PREDISPOSES Acute inflammation
Subject
Peas - dietary
Predicate
PREDISPOSES
Object
Acute inflammation
12. cytokine PRODUCES interleukin-6
Subject
cytokine
Predicate
PRODUCES
Object
interleukin-6
13. Inhibitor PART_OF B-Lymphocytes
Subject
Inhibitor
Predicate
PART_OF
Object
B-Lymphocytes
14. Polypeptides COEXISTS_WITH Inhibitor
Subject
Polypeptides
Predicate
COEXISTS_WITH
Object
Inhibitor
15. Polypeptides STIMULATES B-Lymphocytes
Subject
Polypeptides
Predicate
STIMULATES
Object
B-Lymphocytes
16. Polypeptides ASSOCIATED_WITH Acute Lung Injury
Subject
Polypeptides
Predicate
ASSOCIATED_WITH
Object
Acute Lung Injury
ABSTRACT
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)-1ß, 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.
Subject(s)
Keywords

Full text: Available Collection: International databases Database: MEDLINE Main subject: Palmitic Acids / Cytokines / MAP Kinase Signaling System / Ethanolamines / Acute Lung Injury / Amides Limits: Animals Language: English Year: 2021 Document Type: Article Affiliation country: Ijms22115533

Full text: Available Collection: International databases Database: MEDLINE Main subject: Palmitic Acids / Cytokines / MAP Kinase Signaling System / Ethanolamines / Acute Lung Injury / Amides Limits: Animals Language: English Year: 2021 Document Type: Article Affiliation country: Ijms22115533