• Anticancer research · Jan 2007

    ROS mediates baicalin-induced apoptosis in human promyelocytic leukemia HL-60 cells through the expression of the Gadd153 and mitochondrial-dependent pathway.

    • Hsu-Fung Lu, Shu-Ching Hsueh, Yung-Tsuan Ho, Ming-Ching Kao, Jai-Sing Yang, Tsan-Hung Chiu, Shau-Yen Huamg, Ching-Chung Lin, and Jing-Gung Chung.
    • Department of Clinical Pathology, Cheng Hsin Rehabilitation Medical Center, Taipei, Taiwan, ROC.
    • Anticancer Res. 2007 Jan 1; 27 (1A): 117-25.

    BackgroundChemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of leukemia. In this study, we investigated the effects of baicalin (a compound obtained from Scutellaria baicalensis Georgi and S. rivularis Benth Labiateae) on the viability, induction of apoptosis and associated mechanism in human leukemia HL-60 cells.Materials And MethodsThe cell viability and apoptosis was examined by flow cytometric analysis. The results showed that baicalin induced cytotoxicity in a dose- and time-dependent manner through the activation of caspase-3, as shown by treatment of HL-60 cells with an inhibitor of caspase-3 (z-VAD-fmk). Baicalin increased the levels of ROS, Ca2+ and decreased mitochondrial membrane potential in HL-60 cells. Western blot demonstrated that baicalin promoted the levels of Gadd153, Bax, cytochrome c and caspase-3 and -12, but decreased the levels of Grp78 and Bcl-2 in HL-60 cells.ConclusionBaicalin was found to induce apoptosis in HL-60 cells through multiple pathways.

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