Key result
Urolithin A attenuates AHR-mediated inflammatory signaling in vitro as a direct human-selective antagonist.
Why the study?
The molecular mechanisms underlying the beneficial effects of urolithins, including their anti-inflammatory and anti-cancer effects, remain unclear.
Population
Caco-2 cells and cell-based reporter systems
Comparison
Urolithin A and B vs TCDD or control
Design
Preclinical cell-based experimental study
Authors
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May inform AHR-targeted anti-inflammatory strategies; leaves open translation to human cardiovascular disease.
p-value: p=<0.0001
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 vs. Vehicle or TCDD alone was evaluated on AHR-mediated transcriptional activity and CYP1A1 mRNA levels (p=<0.0001). Urolithin A acts as a direct, human-selective aryl hydrocarbon receptor antagonist that attenuates TCDD-induced AHR-mediated transcriptional activity and inflammatory signaling in vitro.
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