| Objective:To study the mechanism of apoptosis and autophagy induced by curcumin in malignant glioma cells.Methods: The MTT assay was used to determine the cytotoxic effects of curcumin. Cell cycle distribution was analyzed using flow cytometry and apoptosis was assessed using flow cytometry analysis after staining DNA with propidium iodide. The expression of autophagy was monitored with monodansylcadaverin (MDC) staining and Transmission Electron Microscope (TEM) after curcumin treatment. Molecular mechanism was determined using Western blotting analysis.Results: The treatment of curcumin significantly suppressed glioma cells growth in a dose-dependent manner.The results proved that curcumin induced apoptosis in U251 cells, but apoptosis rates of U87 cells were not significantly increased. Curcumin increased the level of autophagy in U87 cells by inhibiting PI3K/AKT signal transduction, upregulated the expression of LC3 and Beclin1, and led to autophagic cell death. It indicated that p53 could inhibit autophagy in U87 cells. Pft-α,a p53 inhibitor, could increase the level of autophagy and synergisticly strengthen the level of autophagy induced by curcumin in U87 cells.Conclusion:Curcumin could significantly suppress the growth of malignant gliomas in vitro. Curcumin promoted cell apoptosis in U251 cells, activated autophagy and induced autophagic cell death in U87 cells. Pft-α, a p53 inhibitor could increase the level of autophagy and synergisticly strengthen the level of autophagy induced by curcumin in U87 cells. |