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Tytuł pozycji:

Dehydrodieugenol improved lung inflammation in an asthma model by inhibiting the STAT3/SOCS3 and MAPK pathways.

Tytuł:
Dehydrodieugenol improved lung inflammation in an asthma model by inhibiting the STAT3/SOCS3 and MAPK pathways.
Autorzy:
Santana FPR; Department of Biological Science, Federal University of São Paulo, Diadema, SP, Brazil; Department of Medicine, School of Medicine, University of São Paulo, SP, Brazil.
da Silva RC; Department of Biological Science, Federal University of São Paulo, Diadema, SP, Brazil.
Ponci V; Department of Biological Science, Federal University of São Paulo, Diadema, SP, Brazil.
Pinheiro AJMCR; Universidade CEUMA, São Luís, MA, Brazil; Programa de Pós-Graduação da Rede BIONORTE, Brazil.
Olivo CR; Department of Medicine, School of Medicine, University of São Paulo, SP, Brazil.
Caperuto LC; Department of Biological Science, Federal University of São Paulo, Diadema, SP, Brazil.
Arantes-Costa FM; Department of Medicine, School of Medicine, University of São Paulo, SP, Brazil.
Claudio SR; Department of Bioscience, Federal University of São Paulo, Santos, Brazil.
Ribeiro DA; Department of Bioscience, Federal University of São Paulo, Santos, Brazil.
Tibério IFLC; Department of Medicine, School of Medicine, University of São Paulo, SP, Brazil.
Lima-Neto LG; Universidade CEUMA, São Luís, MA, Brazil; Programa de Pós-Graduação da Rede BIONORTE, Brazil.
Lago JHG; Center of Natural Sciences and Humanities, Federal University of ABC, Santo André, SP, Brazil.
Prado CM; Department of Bioscience, Federal University of São Paulo, Santos, Brazil. Electronic address: .
Źródło:
Biochemical pharmacology [Biochem Pharmacol] 2020 Oct; Vol. 180, pp. 114175. Date of Electronic Publication: 2020 Jul 24.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: Oxford : Elsevier Science
Original Publication: Oxford, New York [etc.] Paragamon Press.
MeSH Terms:
Asthma/*drug therapy
Eugenol/*analogs & derivatives
Lignans/*therapeutic use
MAP Kinase Signaling System/*drug effects
Pneumonia/*drug therapy
STAT3 Transcription Factor/*antagonists & inhibitors
Suppressor of Cytokine Signaling 3 Protein/*antagonists & inhibitors
Animals ; Asthma/metabolism ; Dose-Response Relationship, Drug ; Eugenol/isolation & purification ; Eugenol/pharmacology ; Eugenol/therapeutic use ; Lauraceae ; Lignans/isolation & purification ; Lignans/pharmacology ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Mice, Inbred BALB C ; Plant Extracts/isolation & purification ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Pneumonia/metabolism ; RAW 264.7 Cells ; STAT3 Transcription Factor/metabolism ; Suppressor of Cytokine Signaling 3 Protein/metabolism
Contributed Indexing:
Keywords: Asthma; Dehydrodieugenol; Eugenol; MAPK; STAT
Substance Nomenclature:
0 (Lignans)
0 (Plant Extracts)
0 (STAT3 Transcription Factor)
0 (Socs3 protein, mouse)
0 (Stat3 protein, mouse)
0 (Suppressor of Cytokine Signaling 3 Protein)
0 (dehydrodieugenol)
3T8H1794QW (Eugenol)
Entry Date(s):
Date Created: 20200728 Date Completed: 20201231 Latest Revision: 20201231
Update Code:
20240104
DOI:
10.1016/j.bcp.2020.114175
PMID:
32717226
Czasopismo naukowe
Background: Eugenol, a common phenylpropanoid derivative found in different plant species, has well-described anti-inflammatory effects associated with the development of occupational hypersensitive asthma. Dehydrodieugenol, a dimeric eugenol derivative, exhibits anti-inflammatory and antioxidant activities and can be found in the Brazilian plant species Nectandra leucantha (Lauraceae). The biological effects of dehydrodieugenol on lung inflammation remain unclear.
Purpose: This study aimed to investigate the effects of eugenol and dehydrodieugenol isolated from N. leucantha in an experimental model of asthma.
Methods: In the present work, the toxic effects of eugenol and dehydrodieugenol on RAW 264.7 cells and their oxidant and inflammatory effects before lipopolysaccharide (LPS) exposure were tested. Then, male BALB/c mice were sensitized with ovalbumin through a 29-day protocol and treated with vehicle, eugenol, dehydrodieugenol or dexamethasone for eight days beginning on the 22nd day until the end of the protocol. Lung function; the inflammatory profile; and the protein expression of ERK1/2, JNK, p38, VAChT, STAT3, and SOCS3 in the lung were evaluated by immunoblotting.
Results: Eugenol and dehydrodieugenol were nontoxic to cells. Both compounds inhibited NO release and the gene expression of IL-1β and IL-6 in LPS-stimulated RAW 264.7 cells. In OVA-sensitized animals, dehydrodieugenol reduced lung inflammatory cell numbers and the lung concentrations of IL-4, IL-13, IL-17, and IL-10. These anti-inflammatory effects were associated with inhibition of the JNK, p38 and ERK1/2, VAChT and STAT3/SOCS3 pathways. Moreover, treatment with dehydrodieugenol effectively attenuated airway hyperresponsiveness.
Conclusion: The obtained data demonstrate, for the first time, that dehydrodieugenol was more effective than eugenol in counteracting allergic airway inflammation in mice, especially its inhibition of the JNK, p38 and ERK1/2, components of MAPK pathway. Therefore, dehydrodieugenol can be considered a prototype for the development of new and effective agents for the treatment of asthmatic patients.
(Copyright © 2020 Elsevier Inc. All rights reserved.)

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