Emodin induces leukemic HL-60 cells apoptosis probably by inhibiting Akt signal pathway.
- Author:
He-yong ZHENG
1
;
Jian-da HU
;
Zhi-hong ZHENG
;
Lü-ye HUANG
;
Ying-yu CHEN
;
Jing ZHENG
;
Xin-ji CHEN
;
Lian-huang LÜ
Author Information
1. Union Hospital of Fujian Medical University, Fujian Institute of Hematology, Fuzhou 350001, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Proliferation;
drug effects;
Dose-Response Relationship, Drug;
Emodin;
pharmacology;
HL-60 Cells;
Humans;
I-kappa B Proteins;
metabolism;
NF-KappaB Inhibitor alpha;
Protein Kinases;
metabolism;
Proto-Oncogene Proteins c-akt;
metabolism;
Signal Transduction;
drug effects;
TOR Serine-Threonine Kinases;
Transcription Factor RelA;
metabolism
- From:
Acta Pharmaceutica Sinica
2007;42(11):1142-1146
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate the effect of emodin on inducing human myeloid leukemia cell line HL-60 apoptosis and the role of Akt signal pathway in the apoptosis. HL-60 cells were exposed to various dosages of emodin. MTT assay was used to detect HL-60 cell proliferation. Distribution of HL-60 cells in cell cycle was analyzed by flow cytometry and cell apoptosis was observed by MitoCapture apoptosis detection. The protein expressions of Akt signal pathway were detected by Western blotting. The result showed that emodin remarkably inhibited the cell proliferation. The IC50 value for 48 h treatment was about 20 micromol x L(-1). Apoptosis in HL-60 cells could be efficiently induced by emodin in a dose dependent manner and cells were arrested at G0/G1. The expressions of Akt, p-Akt, IkappaB-alpha, p-IkappaB-alpha, p65, p-p65, mTOR and p-mTOR in Akt signal pathway were downregulated after emodin treatment. It can be concluded that emodin could efficiently induce growth inhibition and apoptosis in HL-60 cells. Akt signal pathway may be involved in this process.
