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together. Our previous study demonstrated that intracellular shikonin the F Ability, big e quantities of Ren reactive oxygen species in the early stages of the apoptotic process, produce, and has then by St Tion of mitochondrial transmembrane potential in hepatoma SK Hep communicate 1 cells .6 For accompanied This suggests that ROSmediated oxidative stress induced by shikonin, the critical event in the induction of apoptosis in hepatoma SK Hep 1 cells involved kommunizieren.6Denn an enormous amount of data show that shikonin can induce apoptosis in a broad spectrum of human cancer cells lines.7 13 Despite these promising results, the molecular mechanism underlying wherein shikonin exerts its potential not completely antiglioma understood ndig. To Gain a better determine the molecular effects of shikonin ndnis glioma cells, to win with the aim of this study was whether shikonin induces apoptosis in three human glioma cell lines: U87MG, Hs683 and M059K. We focus on two main conclusions focus: first, the events shikoninmediated proapoptotic and the other is the potential mechanism and exact sequence of shikonin-induced apoptosis of glioma cells with high quality. Materials and Methods Cell lines and reagents three human glioma cell lines, U87MG, Hs683 and M059K, were obtained from Bioresource Collection and Research Center. Human astrocytes were purchased from Sciencell. Diacetate and Chloromethylflourescein HamF Tr Hunters 12 were purchased from Invitrogen.