CAJ | 학술논문

Objective: To explore the effects of dexamethasone (DXM) and vincristine (VCR) on cytosine arabinoside (Ara-C) induced apoptosis and activation of nuclear factor-κ-gene binding (NF-κB) in leukemic cell line HL60-n. Methods: Apoptosis of HL60-n cells was analysed by TdT-mediated X-dUTP nick and end labeling (TUNEL) and DNA electrophoresis. NF-κB activity of HL60-n cells was detected by electrophoretic mobility shift assay (EMSA). Results: There was slight activation of NF-κB in HL60-n cells without drug induction. Ara-C at 1 μmol/L significantly enhanced the activation of NF-κB in HL60-n cells. The level of NF-κB activation induced by DXM at 1 μmol/L or VCR at 0.1 μmol/L had no significant difference compared with that of the control group. However, in HL60-n cells pre-treated with 1 μmol/L of DXM or 0.1 μmol/L of VCR, the activation of NF-κB induced by 1 μmol/L of Ara-C was significantly suppressed with inhibition rates of 31.0% and 47.0%, respectively. The apoptosis rates of HL60-n cells induced by 1.0 μmol/L, 10 μmol/L and 100 μmot/L Ara-C were 45.00±3.16%, 61.88±3.40% and 77.62±4.75%, respectively. The apoptotic rates of HL60-n cells induced by DXM at 1 μmol/L or VCR at 0.1 μmol/L were similar to that of the control group. However, either DXM at 1 μmol/L or VCR at 0.l μmol/L could enhance the apoptosis of HL60-n cells induced by Ara-C at 1 μmol/L with rates of 39.1% and 59.2%, respectively. Conclusion: Ara-C can induce apoptosis and activation of NF-κB in HL60-n cells. The mechanism of increased apoptosis of HL60-n cells by DXM or VCR may be related to suppression of NF-κB activation.