Study on mechanism of apoptosis of HL-60 cells induced by cytarabine.
- Author:
Li-Rong SUN
1
;
Bin-Chang GAO
Author Information
1. Department of Paediatrics, Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, China.
- Publication Type:Journal Article
- MeSH:
Antimetabolites, Antineoplastic;
pharmacology;
Apoptosis;
drug effects;
Cytarabine;
pharmacology;
DNA Fragmentation;
drug effects;
HL-60 Cells;
Humans;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
Time Factors;
bcl-2-Associated X Protein;
biosynthesis
- From:
Journal of Experimental Hematology
2005;13(4):575-578
- CountryChina
- Language:Chinese
-
Abstract:
To study the mechanism of apoptosis of HL-60 cells induced by cytarabine (Ara-C), morphological changes of the HL-60 cells stained with Giemsa were observed by microscopy; the DNA fragments were detected by agarose gel electrophoresis; the expressions of Bcl-2 and bax gene-related apoptosis were investigated by immunohistochemistry. The results showed that HL-60 cells in experimental groups had changed in morphology since they were cultured for 8 hours. HL-60 cells stained with Giemsa showed that their nuclear membranes were splitted. The purplish red chromatins were concentrated into pieces and apoptosis bodies were formed. The apoptosis rate increased in the experimental groups compared with the control group. The expression of Bcl-2 protein was lower and the expression of Bax protein was higher and the ratio of Bcl-2/Bax proteins in the experimental groups was lower than those in the control group. It is concluded that Ara-c can effectively induce apoptosis of HL-60 cells and simultaneously decrease the level of expression of Bcl-2 protein and elevate the level of expression of Bax protein. Decrease of expression ratio of Bcl-2/Bax proteins may be one of the main mechanisms in HL-60 apoptosis induced by Ara-C.
