biostudies-literatureNguyen PTThe ministry of education, culture, sports, science and technology, Japan9997https://www.ebi.ac.uk/biostudies/studies/S-EPMC10297944biostudies-literatureUnknown24(12)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. NoInternational journal of molecular sciencesEthyl Caffeate Can Inhibit Aryl Hydrocarbon Receptor (AhR) Signaling and AhR-Mediated Potentiation of Mast Cell Activation.PMC1029794422K19427Nakano NTran NQVNguyen PTNakamura YKobayashi YOkuda TIshimaru KNakao AWatanabe-Saito FNguyen TAfalseEthyl Caffeate Can Inhibit Aryl Hydrocarbon Receptor (AhR) Signaling and AhR-Mediated Potentiation of Mast Cell Activation.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. No2023-01-01T00:00:00Z2023 Jun2025-07-06T03:05:47.775Z2025-04-19T09:00:58.641ZS-EPMC102979443737314410.3390/ijms24129997