Ginsenosides of the 20(S)-protopanaxadiol and 20(S)-protopanaxatriol classifications
including the aglycones, protopanaxadiol (PD), protopanaxatriol (PT), and ginsenosides
Rh2 and Rh1 were shown to posses characteristic effects on the proliferation of human
leukemia cells (THP-1). A similar efficacy was not apparent for ginsenoside Rg3. The
concentrations to inhibit 50% of cells (LC50) for PD, Rh2, PT, and Rh1 were 13, 15,
19, and 210 microg/mL, respectively. PD and PT induced DNA fragmentation at the LC50
after 72 h of treatment, compared to Rh2, Rh1, dexamethasone, and untreated cells.
Cell-cycle analysis confirmed apoptosis with PD and PT treatment of THP-1 cells resulting
in a buildup of sub-G1 cells after 24, 48, and 72 h of treatment. Rh2 and dexamethasone
treatments also increased apoptotic cells after 24 h, whereas Rh1 did not. After 48
and 72 h, Rh2, Rh1, and dexamethasone similarly increased apoptosis, but these effects
were significantly (P<0.05) lower than those observed for both PD and PT treatments.
Furthermore, treatments that produced the largest buildup of apoptotic cells were
also found to have the largest release of lactate dehydrogenase. It can be concluded
from these studies that the presence of sugars in PD and PT aglycone structures reduces
the potency to induce apoptosis, and alternately alter membrane integrity. These cytotoxic
effects were different to THP-1 cells than dexamethasone.