TF-1 cell apoptosis-inducing effect of matrine and its effect on SALL4 expression.
- Author:
Yichuan YU
1
;
Lan WANG
;
Leihua FU
;
Chenlin HU
;
Lin CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Alkaloids; pharmacology; Antineoplastic Agents, Phytogenic; pharmacology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Gene Expression; drug effects; Humans; Leukemia, Erythroblastic, Acute; drug therapy; genetics; metabolism; physiopathology; Quinolizines; pharmacology; Transcription Factors; genetics; metabolism
- From: China Journal of Chinese Materia Medica 2011;36(19):2719-2722
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of matrine (Mat) induced human erythroleukemia TF-1 cell apoptosis and its effect on SALL4 expression.
METHODDifferent concentrations of the Mat (0.5, 1.0, 1.5, 2.0 g x L(-1) ) were cultured in vitro in TF-1 cells at different time (24, 48, 72 h). Cell proliferation was assayed by MTT. Cell cycle was determined by flow cytometry (FCM). Cell apoptosis was detected by Annexin V and PI double staining method. SALL4 mRNA expression was detected by reverse transcription RT-PCR (RTT-PCR).
RESULTAdministrated with Mat (0.5-2.0 g x L(-1)) after 24, 48, 72 h, the proliferation of TF-1 cells were inhibited (P < 0.01) , and in dose- and time-dependent manner. Half inhibitory concentration (IC50 ) was 1.0 g L(-1) at 48 h. After 48 h that the Mat acted on TF-1 cells, the proportion of G0/G1 phase cells increased while compared with the control group, and S phase cells decreased (P < 0.01). Apoptosis were 8.6% , 11.21%, 15.26% , 17.63%, which showed statistically significant difference (P < 0.01) compared with the control group (5.05%). RT-PCR results showed the ratio between SALL4 mRNA expression and beta-actin (internal reference) expression significantly decreased (P < 0.01) with Mat dose increased.
CONCLUSIONIn a certain range of concentration and time, Mat can inhibit TFT-1 cells proliferation. The mechanism is to make the cells G0/G1 phase blocked, to inhibit SALL4 gene expression and induce cell apoptosis.
