OBJECTIVE: To study the effect of embelin on proliferation, differentiation and apoptosis of HL-60 cells and explore its possible mechanism. METHODS: Different concentration of embelin were used to treat HL-60 cells. Cell growth curve was analysed by MTT assay, cell apoptosis by Annexin V/PI double staining and JC-1 dye. The differentiation of HL-60 cells was evaluated by expression of CD33, CD34, CD11b and CD14. Bone marrow cells (BMC) from nine patients with acute nonlymphocytic leukemia (ANML) were also studied. RESULTS: Embelin induced differentiation of HL-60 cells with significant increase of CD14 and CD11b expression at 33.97µmol/L for 3 days (P < 0.01). Embelin induced apoptosis of HL-60 cells in a time- and dose-dependent manner, the apoptosis rates were (9.23 ± 0.05)%, (25.86 ± 0.30)% and (39.03 ± 0.07)% respectively at 339.67 µmol/L of embelin for 12-, 24- and 48-hours treatment (P < 0.05); the apoptosis rates were (0.07 ± 0.03)%, (7.43 ± 0.30)%, (14.01 ± 0.01)%, (25.52 ± 0.03)% and (39.15 ± 0.01)% respectively at 10.19, 33.97, 101.90, 339.67 and 1019.02 µmol/L of embelin for 24-hours culture (P < 0.05). Clusters of differentiation antigen on BMC from three acute promyelocytic leukemia patients showed significant changes at 33.97 µmol/L of embelin treatment for 3 days. Embelin induced apoptosis of BMCs from all the nine ANML patients at 33.97 µmol/L for 24 hour. CONCLUSION: Embelin can inhibit proliferation and induce differentiation and apoptosis of HL-60 cells. The mechanism may be related to mitochondrial apoptosis pathway. Embelin at subtoxic concentration doesn't promote leukemia BMC differentiation, but at 339.67 µmol/L induces apoptosis of these cells.
OBJECTIVE: To study the effect of embelin on proliferation, differentiation and apoptosis of HL-60 cells and explore its possible mechanism. METHODS: Different concentration of embelin were used to treat HL-60 cells. Cell growth curve was analysed by MTT assay, cell apoptosis by Annexin V/PI double staining and JC-1 dye. The differentiation of HL-60 cells was evaluated by expression of CD33, CD34, CD11b and CD14. Bone marrow cells (BMC) from nine patients with acute nonlymphocytic leukemia (ANML) were also studied. RESULTS: Embelin induced differentiation of HL-60 cells with significant increase of CD14 and CD11b expression at 33.97µmol/L for 3 days (P < 0.01). Embelin induced apoptosis of HL-60 cells in a time- and dose-dependent manner, the apoptosis rates were (9.23 ± 0.05)%, (25.86 ± 0.30)% and (39.03 ± 0.07)% respectively at 339.67 µmol/L of embelin for 12-, 24- and 48-hours treatment (P < 0.05); the apoptosis rates were (0.07 ± 0.03)%, (7.43 ± 0.30)%, (14.01 ± 0.01)%, (25.52 ± 0.03)% and (39.15 ± 0.01)% respectively at 10.19, 33.97, 101.90, 339.67 and 1019.02 µmol/L of embelin for 24-hours culture (P < 0.05). Clusters of differentiation antigen on BMC from three acute promyelocytic leukemiapatients showed significant changes at 33.97 µmol/L of embelin treatment for 3 days. Embelin induced apoptosis of BMCs from all the nine ANML patients at 33.97 µmol/L for 24 hour. CONCLUSION: Embelin can inhibit proliferation and induce differentiation and apoptosis of HL-60 cells. The mechanism may be related to mitochondrial apoptosis pathway. Embelin at subtoxic concentration doesn't promote leukemia BMC differentiation, but at 339.67 µmol/L induces apoptosis of these cells.