This study investigated the mechanism underlying the effect of tripterine on apoptosis of human acute myelocytic leukemic cells (HL-60). The apoptosis of HL-60 cells after treatment with triperine of different dosages and durations were determined using flow cytometry and transmission electron microscopy. The expressions of Fas, FasL and NF-κB in the HL-60 cells treated with 1.5 μmol/L tripterine for different durations were measured by flow cytometry. Our results showed treatment with 0.5 ~ 2.5 μmol/L tripterine for 24 h could induce apoptosis of HL-60 cells to different extents (apoptotic rate: 6.13 ~ 36.71%) in which the maximal apoptotic rate was observed after 1.5 μmol/L tripterine treatment for 24 h. In addition, 1.5 μmol/L tripterine could cause gradually increased apoptotic rates in a time-dependent manner presenting typical apoptotic morphology in the HL-60 cells. In the 1.5 μmol/L tripterine-treated HL-60 cells, the number of Fas and FasL positive cells was significantly increased (P < 0.05) accompanied by a markedly decreased number of NF-κB positive cells (P < 0.05), which was in a time dependent manner. Tripterine could effectively induce apoptosis of HL-60 cells and its antitumor mechanism may be related to both the up-regulation of Fas and FasL and down-regulation of NF-κB.
Key words: Tripterine, HL-60 cells, apoptosis, Fas/FasL, NF-κB, regulation.
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