Health human volunteers received a 400 mg oral dose of chrysin. Peak plasma chrysin concentrations were only 3-16 ng/ml with AUCs of 5-193 ng/ml h. Plasma chrysin sulfate concentrations were 30-fold higher (AUC 450-4220 ng/ml h). In urine, chrysin and chrysin glucuronide accounted for 0.2-3.1 mg and 2-26 mg, respectively. Most of the dose appeared in feces as chrysin. These findings suggest that chrysin has low bioavailability.

AGS human gastric cancer cell line was cultured in RPMI-1640 supplemented with 10% fetal bovine serum and 0.6% penicillin-streptomycin at 37 deg-C in a 5% CO2 atmosphere. Cells were pre-treated with various concentrations of chrysin (10, 20, 30, 50, 80, 100 micro-M) and then treated with PMA. The level of MMP-9 messenger RNA (mRNA) was determined by reverse transcription-PCR. The role of the specific signaling pathways in the PMA-induced MMP-9 expression was examined by pretreating the AGS cells with the ERK 1/2 inhibitor PD98059, the JNK inhibitor SP600125, the p38 MAPK inhibitor SB203580, and chrysin for 1 hour before stimulation with PMA. The PMA-stimulated MMP-9 was inhibited by chrysin in a dose-dependent manner. Chrysin treatments with inhibitors suggest that chrysin may exert at least part of its anticancer effect by controlling MMP-9 expression through suppression of AP-1 activity via a block of the JNK1/2 and ERK1/2 signaling pathways in gastric cancer AGS cells.