{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nguyen PT"],"funding":["The ministry of education, culture, sports, science and technology, Japan"],"pagination":["9997"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10297944"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(12)"],"pubmed_abstract":["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 <i>CYP1A1</i>. EC also inhibited the FICZ-induced downregulation of AhR expression and DHNA-induced IL-6 production in BMMCs. Furthermore, the pretreatment of mice with orally administered EC inhibited DHNA-induced <i>CYP1A1</i> expression in the intestine. No"],"journal":["International journal of molecular sciences"],"pubmed_title":["Ethyl Caffeate Can Inhibit Aryl Hydrocarbon Receptor (AhR) Signaling and AhR-Mediated Potentiation of Mast Cell Activation."],"pmcid":["PMC10297944"],"funding_grant_id":["22K19427"],"pubmed_authors":["Nakano N","Tran NQV","Nguyen PT","Nakamura Y","Kobayashi Y","Okuda T","Ishimaru K","Nakao A","Watanabe-Saito F","Nguyen TA"],"additional_accession":[]},"is_claimable":false,"name":"Ethyl Caffeate Can Inhibit Aryl Hydrocarbon Receptor (AhR) Signaling and AhR-Mediated Potentiation of Mast Cell Activation.","description":"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 <i>CYP1A1</i>. EC also inhibited the FICZ-induced downregulation of AhR expression and DHNA-induced IL-6 production in BMMCs. Furthermore, the pretreatment of mice with orally administered EC inhibited DHNA-induced <i>CYP1A1</i> expression in the intestine. No","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2025-07-06T03:05:47.775Z","creation":"2025-04-19T09:00:58.641Z"},"accession":"S-EPMC10297944","cross_references":{"pubmed":["37373144"],"doi":["10.3390/ijms24129997"]}}