Ginsenoside Rh2 inhibits proliferation and promotes apoptosis of leukemia KG1-α cells. - GreenMedInfo Summary
[Ginsenoside Rh2 inhibits proliferation and promotes apoptosis of leukemia KG1-α cells].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Jun ;30(6):565-8. PMID: 24909273
OBJECTIVE: To investigate the effect of ginsenoside Rh2 on leukemia KG1-α cells.
METHODS: KG1-α cells were cultured in 96-well plate and harvested in the exponential phase. The cells were induced in the presence of different concentrations of Rg1, Rb1, Rh2 respectively for 24, 48, 72 hours. The conventional culture was performed in blank control group, and cytarabine hydrochloride as the positive control. The inhibitory effects of ginsenoside Rb1, Rg1, Rh2 on the growth of KG1-α cells were tested by CCK-8 assay. Then the most efficient ginsenoside was chosen for the further study by IC50. The effects of the ginsenoside Rh2 on cell cycle and apoptosis were detected by flow cytometry (FCM) combined with PI staining and annexin V-FITC/PI, respectively. The expressions of P53, P21, cyclin D1 and cleaved-caspase-3 were examined by Western blotting.
RESULTS: CCK-8 assay results showed that IC50 of ginsenoside Rh2, ginsenoside Rb1, ginsenoside Rg1 and cytarabine were 75, 207, 268, 1058μmol/L, respectively. Compared with those in blank control group, the KG1-α cells after treated with 75 μmol/L ginsenoside Rh2 showed up-regulated apoptosis rates from (5.37±0.02)% to (8.37±0.015)% at 24 hours and to (33.22±1.67)% at 48 hours (P<0.05). In addition, the percentage of cells in G0/G1 phase increased significantly from (26.78±3.14)% to (29.26±2.31)% at 24 hours and to (44.77±2.26)% at 48 hours, and the percentage in S phase decreased significantly from (65.43±2.22)% to (51.46±0.57)% and (48.29±1.80)%, respectively. The expression levels of cleaved-caspase 3, P53 and P21 proteins went up significantly when the cells were treated with 75 μmol/L Rh2(P<0.05), meanwhile cyclin D1 protein dropped significantly (P<0.05).
CONCLUSION: Ginsenoside Rh2 could inhibit the proliferation of KG1-α cell and prompt its apoptosis.