Objective      To investigate the role and mechanism of dihydroartemisinin in inducing apoptosis in glioma GL261 cells.       Methods      GL261 cells were treated with different concentrations of dihydroartemisinin (0

30

60 and 90 μmol/L). The morphological changes of GL261 were observed by an inverted microscope

and the viability of GL261 cells was measured by CCK-8 assay. Annexin V PI assay was used to study the percentage of apoptotic GL261 cells. Laser scanning confocal microscopy was applied to examine the expression and subcellular localization of activated caspase-3 in the GL261 cells

and Western blotting was carried out to detect the expression of ac

tivated caspase-3 and Bcl-xL.       Results      Dihydroartemisinin reduced the viability and induced apoptosis of GL261 cells in a dose-dependent manner (

P

0.05). Treatment with 30 μmol/L dihydroartemisinin for 12 h could induce the activation of caspase-3 and co-localization with the nucleus in GL261 cells. Dihydroartemisinin could up-regulate the level of activated caspase-3 and down-regulate the level of Bcl-xL in GL261 cells in a dose-dependent manner (

P

0.05).       Conclusion      Dihydroartemisinin induces apoptosis in GL261 cells. Anti-apoptotic protein Bcl-xL and the executor caspase-3 are involved in this process.