Effect of emodin on induction of apoptosis in jurkat cells and its possible mechanisms.
- Author:
Tian-Nan WEI
1
;
Jian-Da HU
;
Ying-Yu CHEN
;
Xin-Ji CHEN
;
Ting-Bo LIU
;
Lian-Huang LÜ
Author Information
1. Fujian Institute of Hematology, Union Hospital, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspases;
metabolism;
Cell Proliferation;
drug effects;
Emodin;
metabolism;
pharmacology;
Humans;
Jurkat Cells
- From:
Journal of Experimental Hematology
2009;17(5):1203-1206
- CountryChina
- Language:Chinese
-
Abstract:
The aim of study was to investigate the effect of a traditional Chinese medicine, emodin, on proliferation and apoptosis in T lymphocytic leukemic cell line Jurkat and its mechanisms. Cell proliferation inhibition was detected by MTT assay. Cell apoptosis was measured by DNA ladder and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. The expressions of related proteins and caspase family members were determined by Western blot. The results showed that emodin inhibited proliferation in Jurkat cells, with an IC50 about 20 micromol/L and induced cell apoptosis in both time-and dose-dependent manners. The expressions of proliferation-related protein C-MYC, hTERT and apoptosis-related protein BCL-2 were down-regulated in a time dependent manner after the treatment with emodin. The expressions of procaspase-3, -8 and -9 all decreased while activated caspase-3 and PARP expressions were up-regulated. It is concluded that emodin can remarkably inhibit cell proliferation and induce apoptosis in Jurkat cells. The down-regulation of proliferation-related proteins C-MYC, hTERT and apoptosis-related protein BCL-2 expressions and activation of caspase cascade may be involved in the process of apoptosis.
