We examined the modulation of protein kinase C (PKC) subtypes during apoptosis induced by ginsenoside Rh2 (G-Rh2) in human neuroblastoma SK-N-Bl(2) and rat glioma C6Bu-1 cells. Apoptosis induced by C-Rh2 in both cell lines was confirmed, as indicated by DNA fragmentation and in situ strand breaks, and characteristic morphological changes. During apoptosis induced by G-Rh2 in SK-N-BE(2) cells, PKC subtypes $alpha$, $eta$ and $gamma$ were progressively increased with prolonged treatment, whereas PKC $delta$ increased transiently at 3 and 6 h and PKC $varepsilon$ was gradually down-regulated after 6 h following the treatment. On the other hand, PKC subtype $eta$ markedly increased at 24 h when maximal apoptosis was achieved. In C6Bu-l cells, no significant changes in PKC subtypes $alpha$, $gamma$, $delta$, $varepsilon$ and $eta$ were observed during apoptosis induced by G-Rh2. These results suggest the evidence for a possible role of PKC subtype in apoptosis induced by G-Rh2 in SK-N-BE(2) cells but not in C6Bu-1 cells, and raise the possibility that G-Rh2 may induce apoptosis via different pathways interacting with or without PKC in different cell types.