Effects of emodin on human erythroleukemia cell line HEL.
- Author:
Xu-Chun HE
1
;
Jian-Da HU
Author Information
1. Fujian Hygienic Professional Technology College, Fuzhou, Fujian Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Emodin;
pharmacology;
Glycogen Synthase Kinase 3;
metabolism;
Glycogen Synthase Kinase 3 beta;
HSP70 Heat-Shock Proteins;
metabolism;
Humans;
Leukemia, Erythroblastic, Acute;
metabolism;
pathology;
Proto-Oncogene Proteins c-akt;
metabolism
- From:
Journal of Experimental Hematology
2011;19(5):1121-1124
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the inhibitory effect of emodin on the proliferation of HEL cells, the inducing apoptosis effect of HEL cells and their mechanisms. The proliferation inhibition was detected by MTT method; the change of morphology was observed by AO/EB stains; the cell cycle and apoptosis was analyzed by flow cytometry; the expressions of Akt, P-Akt, P-GSK3β and HSP70 proteins were determined by Western blot. The results indicated that emodin displayed significant anti-proliferative effect on HEL cells in a dose dependent manner(r = 0.99), with IC(50) value of 4.19 µmol/L; AO/EB stains showed that the morphology of HEL cells obviously changed after emodin treatment for 24 hours, and at 24 and 48 hours the apoptosis rates of HEL cells treated by emodin were (27.35 ± 1.68)% and (58.49 ± 1.55)% respectively. Compared with blank control group, the cell ratio in G(0)/G(1) phase increased while that in S phase decreased (p < 0.01); the expression of Akt protein was not changed (p > 0.05), and that of P-Akt, P-GSK3β and HSP70 proteins were down-regulated (p < 0.05). It is concluded that emodin efficiently inhibits the HEL cell proliferation and induces apoptosis of HEL cells, which may be related to the down-regulation of P-Akt, P-GSK3β and HSP70 proteins expression.
