Key result
Urolithin A attenuates TCDD-induced inflammation and transcriptional activity in Caco-2 cells via selective AHR antagonism.
Why the study?
The molecular mechanisms underlying the beneficial effects of urolithins, including their anti-inflammatory activity, remain unclear and may involve the aryl hydrocarbon receptor (AHR).
Population
Cell-based reporter system and Caco-2 cells
Comparison
Urolithin A and B versus TCDD-induced AHR activity or vehicle
Design
Preclinical experimental study
Authors
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Hypothesis-generating for urolithin A in AHR-mediated gut inflammation; prospective human trials needed before clinical consideration.
Urolithin A is identified as a dietary microbiota-derived human selective AHR antagonist, providing a molecular mechanism for its anti-inflammatory effects.
Muku et al. (2018) studied this question. Urolithin A and B vs. TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) or unexposed cells was evaluated on AHR-mediated transcriptional activity and CYP1A1 mRNA levels. Urolithin A acts as a direct dietary-derived human selective aryl hydrocarbon receptor antagonist, attenuating TCDD-induced transcriptional activity and inflammatory expression in Caco-2 cells.
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