Ginsenoside Rh2 inhibits human A172 glioma cell proliferation and induces cell cycle arrest status via modulating Akt signaling pathway

Ginsenoside Rh2 (G-Rh2), the main bioactive component in American ginseng, is known to exert a wide variety of biological activities. Accumulating evidence suggests that G-Rh2 inhibits cell proliferation and induces apoptosis of tumor cells. However, the possible mechanism through which G-Rh2 exerts its action on malignant glioma cells have not been completely elucidated. The findings of the present study demonstrated that G-Rh2 decreased the viability of glioma cells in a dose- and time-dependent manner, and induced cell cycle arrest. G-Rh2-induced cell cycle arrest was accompanied by the downregulation of cyclin-dependent kinase 4 and Cyclin E. In addition, G-Rh2 markedly reduced the expression of total- RAC-α serine/threonine-protein kinase (Akt) and the levels of phosphorylated-Akt. These findings provide mechanistic details of how G-Rh2 acts on glioma cells and suggest that G-Rh2 may function as a potential anti-cancer drug for glioma treatment.