尿石素A

Micromolar urolithin A concentrations induces both autophagy and apoptosis. Urolithin A suppresses cell cycle progression and inhibited DNA synthesis in human sw620 colorectal cancer cells.
Urolithin A shows antiproliferative effects and inhibits T24 and Caco-2 cell growth with IC ₅₀ s of 43.9 and 49 μM, respectively.
Urolithin A exerts a dose- and time-dependent significant arrest at G2/M and S phases after treatments with 50 and 100 μM at 24 and 48 h compared to control cells. It induces cell apoptosis with 50 and 100 μM .
Urolithin A shows potent antiproliferative activity on HepG2 cells. When cell death is induced by Urolithin A, the expression of β-catenin, c-Myc and Cyclin D1 are decreased and TCF/LEF transcriptional activation is notably down-regulated. Urolithin A also increases protein expression of p53, p38-MAPK and caspase-3, but suppresses expression of NF-κB p65 and other inflammatory mediators.

The volume of paw edema is reduced at 1 h after oral administration of urolithin A. In addition, plasma in treated mice exhibited significant oxygen radical antioxidant capacity (ORAC) scores with high plasma levels of the unconjugated form at 1 h after oral administration of urolithin A.