Effects of chloroquine diphosphate on proliferation and apoptosis of human leukemic K562 cells.
- Author:
Pei-Du JIANG
1
;
Ying-Lan ZHAO
;
Sheng-Yong YANG
;
Yong-Qiu MAO
;
Yu-Zhu ZHENG
;
Zheng-Guang LI
;
Yu-Quan WEI
Author Information
1. State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan Province, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Cell Proliferation;
drug effects;
Chloroquine;
analogs & derivatives;
pharmacology;
Dose-Response Relationship, Drug;
Down-Regulation;
drug effects;
Humans;
K562 Cells;
Membrane Potentials;
drug effects;
Mitochondria;
drug effects
- From:
Journal of Experimental Hematology
2008;16(4):768-771
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effects of chloroquine diphosphate on the proliferation and apoptosis of human leukemic K562 cells, and to elucidate its possible mechanism of activity. The inhibitory effect of chloroquine diphosphate with different concentrations on K562 cell proliferation was detected by MTT method. Apoptosis was measured by flow cytometry (FCM); morphological analysis of apoptosis was performed after staining with propidium iodide (PI) under fluorescence microscope; cell apoptosis was assessed by the DNA ladder shown agarose gel electrophoresis. After treatment with chloroquine diphosphate, K562 cells were stained by Rhodamine 123 to detect changes in mitochondrial transmembrane potential (DeltaPsim) by FCM. The results showed that the cell viability decreased in dose-dependent manner, following chloroquine diphosphate treatment at different concentrations (1.5625, 3.125, 6.25, 12.5, 25, 50 and 100 micromol/L) for 24, 48 and 72 hours. By FCM analysis, the significant increases of sub-G(1) were observed. DNA ladder was detected and apoptotic nuclei were observed. DeltaPsim decreased in K562 cells after chloroquine diphosphate treatment. It is concluded that the chloroquine diphosphate can inhibit the proliferation of K562 cells and induce cell apoptosis, which may relate to down-regulation of mitochondrial transmembrane potential (DeltaPsim).
