Ethyl Caffeate Can Inhibit Aryl Hydrocarbon Receptor (AhR) Signaling and AhR-Mediated Potentiation of Mast Cell Activation.
IgE
allergy
aryl hydrocarbon receptor
ethyl caffeate
mast cell
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
10 Jun 2023
10 Jun 2023
Historique:
received:
16
05
2023
revised:
06
06
2023
accepted:
08
06
2023
medline:
29
6
2023
pubmed:
28
6
2023
entrez:
28
6
2023
Statut:
epublish
Résumé
Ethyl caffeate (EC) is a natural phenolic compound that is present in several medicinal plants used to treat inflammatory disorders. However, its anti-inflammatory mechanisms are not fully understood. Here, we report that EC inhibits aryl hydrocarbon receptor (AhR) signaling and that this is associated with its anti-allergic activity. EC inhibited AhR activation, induced by the AhR ligands FICZ and DHNA in AhR signaling-reporter cells and mouse bone marrow-derived mast cells (BMMCs), as assessed by AhR target gene expressions such as
Identifiants
pubmed: 37373144
pii: ijms24129997
doi: 10.3390/ijms24129997
pmc: PMC10297944
pii:
doi:
Substances chimiques
Receptors, Aryl Hydrocarbon
0
2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazophenyl)amide
0
ethyl caffeate
76GBB1JU5Y
Cytochrome P-450 CYP1A1
EC 1.14.14.1
Ligands
0
Anti-Inflammatory Agents
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : The ministry of education, culture, sports, science and technology, Japan
ID : 22K19427
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