Abstract
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.