Apoptotic effects of ginsenoside Rh2 on human malignant melanoma A375-S2 cells.

AIM: To study the mechanism of ginsenoside-Rh2 (G-Rh2)-induced growth inhibition
of A375-S2 cells.
METHODS: A375-S2 cell viability and the effect of caspase inhibitors on
G-Rh2-induced apoptosis were measured by crystal violet assay. Changes in
cellular morphology were observed by phase-contrast microscopy.
Apoptosis-specific nucleosomal DNA fragmentation was assayed by agarose gel
electrophoresis. Cell cycle distribution was measured by flow cytometry.
RESULTS: G-Rh2 inhibited the A375-S2 cell growth in concentration- and
time-dependent manners. Caspase family inhibitor,
z-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), caspase-3 inhibitor,
z-Asp-Glu-Val-Asp-fluoromethylketone (z-DEVD-fmk), and caspase-8 inhibitor,
z-Ile-Glu-Asp-fluoromethylketone (z-IETD-fmk), partially inhibited G-Rh2-induced
apoptosis. But caspase-1 inhibitor, Ac-Tyr-Val-Ala-Asp-chloromethyl-ketone
(Ac-YVAD-cmk), did not antagonize G-Rh2 induced-cell death.
CONCLUSION: G-Rh2 suppresses the growth of A375-S2 cells in vitro by inducing
apoptosis. G-Rh2-induced apoptosis is partially dependent on caspase-8 and
caspase-3 pathway in A375-S2 cells. Other apoptotic pathways might be also
related to the induction of apoptosis by G-Rh2.