This paper deals with the inhibitory mechanisms of ginsenoside G-Rh2 on the growth of tumor cells. G-Rh2 significantly inhibited the proliferation of human cervical adenocarcinoma HeLa cells in a time- and dose-dependent manner. G-Rh2 induced apoptotic manifestations in HeLa cells as evidenced by the changes in the cell morphology, the DNA fragmentation and the activation of caspases. Caspase inhibitors, caspase family inhibitor, z-Val-Ala-Asp-fmk(z-VAD-fmk); caspase-1 inhibitor, Ac-Tyr-Val-Ala-Asp-chloromethyl-ketone(Ac-YVAD-cmk); caspase-3 inhibitor, z-Asp-Glu-Val-Asp-fmk(z-DEVE-fmk) and caspase-8 inhibitor, z-Ile-Glu-Asp-fmk(z-IETD-fmk) effectively attenuated G-Rh2-induced cell death. The activities of caspase-1 and caspase-3 were increased in the G-Rh2-induced apoptotic process. However, caspase inhibitors can not inhibit G-Rh-2 induced cell death completely. These results suggest that G-Rh2-induced cell death is mediated by the activation of caspase cascade, but there might be some other pathways for induction of this apoptosis.