The mechanism for dexamethasone-induced apoptosis of NK-92MI cells

Objective:To study the effects of dexamethasone(DEX)on the cytotoxicity and apoptosis of NK-92MI cells and the mechanisms involved.Methods:NK-92MI cells were treated with different doses of DEX.The proliferative rate and cytotoxicity of the NK-92MI cells were detected by MTT colorimetry.The cell apoptotic rate was observed by flow cytometry with Annexin V and propidium iodide(PI)double staining.The expression of apoptosis-related gene,Bcl-2 and Bax was detected by RT-PCR.Results:After treated with 1×10-8mol/L to 1×10-3mol/L of DEX for 24 h,48 h and 72 h,the proliferation of NK-92MI cells was significant inhibited(P0.05).The cytotoxicity of NK-92MI cells was inhibited by 1×10-8mol/L to 1×10-3mol/L of DEX at effector:target ratio of 5∶1 compared with that of the control group(P0.05).DEX induced apoptosis of NK-92MI cells in both time and dose depended manners.Results of RT-PCR showed that,compared with the control group,the expression of Bcl-2 decreased(P0.05),while Bax increased markedly in DEX group(P0.01).Conclusion:DEX can inhibit proliferation of NK-92MI cells and reduce its cytotoxicity,which may be caused by DEX-induced apoptosis of NK-92MI cells.The molecular mechanism of DEX-induced apoptosis of NK-92MI cells may be associated with the increasing expression of Bax/Bcl-2.