Objective   To investigate the intracellular mechanisms by which 3

6-dihydroxyflavone inducing apoptosis of HL-60 cells.    Methods   After the HL-60 cells were treated with 3

6-dihydroxyflavone at the concentration of 5. 10

20 or 40  mol/L

the cells then were inoculated under the selected optimal concentration. The survival rate of HL-60 cells was analyzed using a haemocytometer with standard trypan blue dye exclusion and a CASY cell counter and analyzer. The contents of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD)

catalase (CAT) and glutathione peroxidase (GSH-Px) in the cells were measured by chemochromatometry. The expression of phosphorylation of ERK

JNK and p38MAPK were examined by Western blotting.    Results   The survival rate of HL-60 cells was significantly reduced in a dose- and time-dependent manner after 3

6-dihydroxyflavone treatment. When the dose was over 10  mol/L or the time was longer than 12 h under the concentration of 20  mol/L

significantly decreased survival rate was observed (P0.05

P0.01). When the cells were treated with 20  mol/L 3

6-dihydroxyflavone

the activities of SOD

CAT and GSH-Px reached the lowest in 2 h

and still significantly lower than those of normal control in 24 h (P0.05 or P0.01). While

the content of MDA raised to its summit in 2 h and then gently decreased

but still significantly higher than that of normal control in 24 h (P0.05). The protein of phosphorylation of ERK in HL-60 cells was significantly decreased in 2 h after 20  mol/L 3

6-dihydroxyflavone treatment and then increased to normal level in 24 h. However

the expressions of phosphorylation of JNK and p38MAPK was increased significantly in 2 h (P0.01) and then decreased slowly

but still higher than those of normal control in 24 h.    Conclusion   3

6-dihydroxyflavone significantly decreases the activities of anti-oxidative enzymes and increases the oxidative stress in HL-60 cells

probably through the JNK and MAPK signaling pathways.