Deferoxamine induces apoptosis of HL-60 cells by activating caspase-3.
- Author:
Dao WANG
1
;
Yu-Feng LIU
;
Ying-Chao WANG
Author Information
1. Department of Pediatrics, The Third Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Deferoxamine;
pharmacology;
HL-60 Cells;
Humans;
bcl-2-Associated X Protein;
biosynthesis;
genetics
- From:
Journal of Experimental Hematology
2006;14(3):485-487
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to observe the changes of caspase-3 activity during apoptosis of HL-60 cells induced by an iron chelator, DFO (deferoxamine), and to explore the mechanism underlying apoptosis in HL-60 cells. The HL-60 cells treated with DFO were examined by light microscopy, flow cytometry (FCM) and DNA agarose gel electrophoresis; the activity of caspase-3 was determined by cellular immunohistochemistry; the transcription of the apoptotic gene of bax was detected by hybridization in situ. The results showed that the typical morphological character of apoptosis cells, DNA ladder and FCM assay confirmed that DFO could induce the apoptosis in HL-60 cells. The apoptotic rate increased in dose-and time-dependent manner. When cells had been cultivated with 100 micromol DFO for 12 hours, a few caspase-3 positive cells were found. In the process of time, the rate of caspase-3 positive cells was progressively higher than that in control (P < 0.05), while the level of bax transcription was also higher than that in the control. It is concluded the activation of caspase-3 and gene bax may be involved in the apoptosis of HL-60 cells induced by DFO.
