BACKGROUND:: Domestic and international studies demonstrated that ginsenoside and its monomers inhabit leukemia cells proliferation and increase sensitivity and reversing drug resistance of chemotherapeutics. However, most research regarding ginsenoside is focus on solid tumor and acute leukemia, and the reports concerning chronic leukemia are few. OBJECTIVE:: To investigate the effect of ginsenoside Rb1, Rg1 on proliferation of chronic myelocytic leukemia K562 cells. DESIGN, TIME AND SETTING:: An in vitro cytology observation. The experiment was performed at the Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, Laboratory of Ophthalmology of Chongqing Medical University from March 2008 to March 2009. MATERIALS:: K562 cells were supported by Department of Clinical Laboratory, Chongqing Medical University. ginsenoside Rb1, Rg1 with purity of 98.6% was provided by Estima Institute of Chinese Medicine. METHODS:: The density of K562 cells with logarithmic phase were regulated to 7×10/L and incubated with 20, 40, 80, 160 μmol/L ginsenoside Rb1 or 5, 10, 20, 40, 80 μmol/L ginsenoside Rg1, respectively. The conventional culture was performed in the blank control group. MAIN OUTCOME MEASURES:: The proliferation of K562 cells was examined by MTT and trypan blue staining; meantime, the changes of cell cycle were determined by flow cytometry. RESULTS:: Ginsenoside Rb1, Rg1 inhibited K562 cells proliferation significantly in vitro, which exhibited a dose-dependent manner at range of 20-160 μmol/L Rb1 and 5-20 μmol/L Rg1, and reached peak at hour 48. Compared to the blank control group, there was no cell cycle change in the 160 μmol/L Rb1 group at hour 48 after culture. However, S phase cells in the 20 μmol/L Rg1 group were dramatically increased (P < 0.05), G1 phase cells were decreased (P < 0.05); in addition, no “subdiploid” peak appeared in the 160 μmol/L Rb1 and 20 μmol/L Rg1 groups. CONCLUSION:: Ginsenoside Rb1, Rg1 can inhibit the proliferation of K562 cells in vitro. The inhibitory mechanisms of Rg1 may be arrested cells in S phase. However, the association between Rb1 inhibition and cell cycle still need to be explored.