Figure 1
Figure 1. Wogonin exclusively induces apoptosis in malignant and not in normal T cells. (A,B) Wogonin induces a dose-dependent increase in apoptotic cell death in CEM leukemia T cells. CEM cells were incubated with different doses of Wogonin for 24 hours. Apoptotic changes in cell size and granularity were quantified by a decrease in FSC/SSC (A), and the apoptotic cell death was analyzed by FACS for DNA fragmentation (B). Results are representative of 4 separate experiments, and each experiment was carried out in triplicate. (C) The leukemic T-cell line Molt-4 was treated by different doses of Wogonin, and apoptotic cell death was determined by fluorescence-activated cell sorting (FACS) for DNA fragmentation. Results are representative of 2 separate experiments done in triplicate. (D) Leukemic T-cell lines CEM, Jurkat, and DND-41 and normal T-cell clones K234, D894/25, and D596/6 were treated with different doses of Wogonin for 24 hours. Apoptotic cell death was analyzed by FACS for DNA fragmentation. Results are representative of 2 separate experiments done in triplicate. (E) CEM and normal T cells freshly isolated from peripheral blood of 3 representative healthy donors were treated with 10 to 50 μM (left panel) or 100 μM (right panel) of Wogonin for 24 and 48 hours. (F) Resistance of nonmalignant T cells to Wogonin-induced apoptosis is not dependent on the activation stages of T cells. Freshly isolated peripheral blood T cells (day 0), 16 hours PHA-activated (day 1), or PHA-activated and further cultured in the presence of IL-2 for 5 days (day 6) were treated with Wogonin. Results are representative of 3 donors analyzed in duplicate. Error bars represent SD.

Wogonin exclusively induces apoptosis in malignant and not in normal T cells. (A,B) Wogonin induces a dose-dependent increase in apoptotic cell death in CEM leukemia T cells. CEM cells were incubated with different doses of Wogonin for 24 hours. Apoptotic changes in cell size and granularity were quantified by a decrease in FSC/SSC (A), and the apoptotic cell death was analyzed by FACS for DNA fragmentation (B). Results are representative of 4 separate experiments, and each experiment was carried out in triplicate. (C) The leukemic T-cell line Molt-4 was treated by different doses of Wogonin, and apoptotic cell death was determined by fluorescence-activated cell sorting (FACS) for DNA fragmentation. Results are representative of 2 separate experiments done in triplicate. (D) Leukemic T-cell lines CEM, Jurkat, and DND-41 and normal T-cell clones K234, D894/25, and D596/6 were treated with different doses of Wogonin for 24 hours. Apoptotic cell death was analyzed by FACS for DNA fragmentation. Results are representative of 2 separate experiments done in triplicate. (E) CEM and normal T cells freshly isolated from peripheral blood of 3 representative healthy donors were treated with 10 to 50 μM (left panel) or 100 μM (right panel) of Wogonin for 24 and 48 hours. (F) Resistance of nonmalignant T cells to Wogonin-induced apoptosis is not dependent on the activation stages of T cells. Freshly isolated peripheral blood T cells (day 0), 16 hours PHA-activated (day 1), or PHA-activated and further cultured in the presence of IL-2 for 5 days (day 6) were treated with Wogonin. Results are representative of 3 donors analyzed in duplicate. Error bars represent SD.

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