Objective      To determine the effect of ginsenoside Rg1 on the proliferation and differentiation of chronic myelocytic leukemia K562 cells and investigate the possible underlying molecular mechanisms.       Methods      K562 cells was treated by 20 μmol/L ginsenoside Rg1 for 24

48 and 72 h

and flow cytometry (FCM)

was used to measure the inhibitory proliferation. Wright’s staining and hemoglobinometry were employed to observe the morphology and haemoglobin synthesis to determine the K562 cells differentiation into erythroid cells after the treatment of ginsenoside Rg1. The expression and distribution of signal transducer and activator of transcription 5 (STAT5) in the k562 cells induced by Rg1 were detected by Western blotting and laser confocal microscopy.       Results      There were more K562 cells arrested at S phase after Rg1 treatment

and the cell count reached peak at 48 h (

P

0.05). There were significantly more hemoglobin in K562 cells induced by gensingnoside Rg1 than the cells without treatment (

P

0.05). Wright’s staining indicated that the K562 cells presented as diminished cell body

reduced nuclear size

abundant cytoplasm

and decreased karyoplasmic ratio

indicating that  gensingnoside Rg1 induced the K562 cell differentiation into erythroid cells. Laser confocal microscopy showed the STAT5 green fluorescence was decreased in the cytoplasm

but increased in the nucleus when induced by Rg1. Western blotting analysis showed the expression of STAT5 was increased in the cytoplasm

and decreased in the nucleus when Rg1 was induced for 48 h.       Conclusion      Ginsenoside Rg1 may inhibit the proliferation in K562 cells and induce the cells differentiation into erythroid cells. Rg1 changes the location of STAT5 and decreases the expression of STAT5 in the nucleus of K562 cells

which might be one of the molecular mechanisms of ginsenoside Rg1 on differentiation of K562 cells.