- Author:
Ying YANG
1
;
Rong HU
1
;
Ke ZHU
1
;
Yingchun LI
1
;
Jia LI
1
;
Miao MIAO
1
;
Hongtao WANG
1
;
Kun YAO
1
;
Zhuogang LIU
1
Author Information
- Publication Type:Journal Article
- MeSH: Acetylcysteine; Apoptosis; Benzoquinones; Cell Survival; Comet Assay; DNA Damage; Fluoresceins; HL-60 Cells; Humans; Oxidative Stress; Reactive Oxygen Species
- From: Chinese Journal of Hematology 2015;36(6):465-468
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the effects of Embelin on HL-60 cells by the impact of oxidative stress on DNA double-strain breaks (DSBs).
METHODSHL-60 cells were treated with Embelin in different concentration (3, 10, 30, 100, and 300 μg/ml) for 24 h, and inhibitory effects was examined by CCK-8 assay. Reactive oxygen species (ROS) levels were evaluated by flow cytometry using DCFH-DA. Comet assay was used to detect the extent of DSBs.
RESULTSEmbelin inhibited proliferation of HL-60 cells in a dose-dependent manner. At the concentration of 10, 30, 100, and 300 μg/ml, the inhibition rate was (12.74 ± 2.27)%, (23.49 ± 1.96)%, (30.30±1.89)%, and (57.55 ± 3.59)% (P<0.05). Embelin also lead to high level of intracellular ROS and deterioration of DNA damage (P<0.05). When HL-60 cells were pretreated with ROS scavenger N-acetyl-l-cysteine (NAC) for 2 h and then treated with 300 μg/ml Embelin for 24 h, the intracellular ROS level declined and DSBs relieved (P<0.05). Meanwhile, embelin-induced cell viability significantly declined to (32.75 ± 2.70)% (P<0.05).
CONCLUSIONEmbelin induced the death of HL-60 cells by increasing the generation of intracellular oxidation and the oxidative stress, which drived the damage of DNA double-strand.