Mechanism of apoptosis induced by indole-3-acetic acids combined with horseradish peroxidase in leukemia cell line K562.
- Author:
Ling YANG
1
;
Tu-Sheng SONG
;
Chen HUANG
;
Li-Ying LIU
;
Yu LUO
;
Lei NI
;
Lü-Sheng SI
Author Information
1. Department of Biology and Medical Genetics, Medical College of Xi'an Jiaotong University, Xi'an 710061, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Proliferation;
drug effects;
Cell Survival;
drug effects;
Dose-Response Relationship, Drug;
Drug Synergism;
Horseradish Peroxidase;
pharmacology;
Humans;
In Situ Nick-End Labeling;
Indoleacetic Acids;
pharmacology;
K562 Cells;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
metabolism;
pathology;
Microscopy, Confocal;
Reactive Oxygen Species;
metabolism;
Superoxide Dismutase;
metabolism;
Time Factors
- From:
Journal of Experimental Hematology
2005;13(5):769-773
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the possible mechanism of apoptosis induced by indole-3-acetic acid (IAA) combined with horseradish peroxidase in leukemia cell line K562, cell proliferation and apoptosis of K562 cell were examined by MTT assay and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), respectively; the activity of superoxide dismutase (SOD) and the quantitative change of MDA were measured by biochemical method; changes of free radical were determined by 2, 7-dichlorofluorescin diacetate (DCFH-DA) probe with confocal microscopy. The results showed that of MTT assay and TUNEL indicated that IAA/HRP could significantly inhibit cell proliferation (P < 0.05) and induce apoptosis of K562 cell (P < 0.01), at the same time a positive correlation was found between apoptosis rate and IAA concentration (r = 0.971, P < 0.01). The activity of SOD and the quantitative of MDA increased, accompanied with a rise in IAA concentration. Results detected by DCFH-DA probe indicated that the fluorescence intensity of intracellular free radical increased, as compared with control, and a positive correlation was found. It is concluded that IAA/HRP can inhibit proliferation of K562 cells and induce K562 cell apoptosis, its mechanism may be related with the increase of intracellular free radical due to the effects of IAA/HRP.
