In this study, 10 metabolites were obtained by collecting
and extracting
fecal samples after oral administration of panaxadiol (PD). Of these
10 metabolites, M7 (3β,21β,22α-hydroxy-24-norolean-12-ene),
M8 (21β,22α-hydroxy-24-norolean-12-ene-3-one), M9 (3β,30α-hydroxy-24-norolean-22,30-epoxy-12-ene),
and M10 (3β,21β-hydroxy-24-norolean-12-ene) were new compounds.
MTT screening of the isolated compounds revealed that the inhibitions
of cancer cells by M2, M4, M7, M8, and M10 were significantly stronger
than that by the mother drug M0, with the activity of M2 being the
most significant. Further, we investigated the anticancer mechanism
of M2. The results showed that M2 significantly increased the level
of ROS in cells; regulated the expressions of Bax, Bcl-2, and Cyt-C
through the mitochondrial pathway; triggered the caspase cascade;
and induced apoptosis. M2 could also induce G1 phase arrest and significantly
regulate cell cycle-related proteins. In conclusion, the experimental
results provide data for further study on the metabolic mechanism
of PD in vivo and the potential of developing new anti-cancer drugs.