Inhibition effect of gambogic acid on MUTZ-1 cell line and its possible mechanism / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 373-376, 2009.
Article
en Zh
| WPRIM
| ID: wpr-302130
Biblioteca responsable:
WPRO
ABSTRACT
This study was aimed to investigate the effects of gambogic acid on the cells of high-risk patients with myelodysplastic syndrome (MDS) in vitro and its mechanism. The inhibition effect of gambogic acid on growth of MUTZ-1 cell line of MDS-RAEB was detected by MTT method. Apoptosis and cell cycle were detected by morphological observation and flow cytometry respectively. The expressions of bax/bcl-2 gene at mRNA level were detected by RT-PCR. The results indicated that the Gambogic acid inhibited the growth of MUTZ-1 cells, the inhibitory rate of gambogic acid with the range of 0.2 - 0.8 microg/ml was enhanced along with increasing of drug concentration. Flow cytometric assay showed that the apoptotic rate of MUTZ-1 cells treated by gambogic acid also was enhanced along with increasing of drug concentration, the apoptotic rates resulting from gambogic acid (0, 0.4, 0.6, 0.8 microg/ml) were (5 +/- 0.5)%, (13 +/- 0.5)%, (37 +/- 0.7)% and (56 +/- 0.6)% respectively. The characteristic changes of apoptosis emerged in MUTZ-1 cells after being exposed to gambogic acid. Gambogic acid could significantly down-regulate the expressions of bcl-2 gene in a dose dependent manner, however, it had no effects on bax gene. It is concluded that within the range of concentration from 0.4 to 0. 8 microg/ml, gambogic acid can inhibit the growth of MUTZ-1 cells by inducing their apoptosis and down-regulating the expression of bcl-2 gene, which may be one of the main mechanisms underlying its antitumor effects.
Texto completo:
1
Base de datos:
WPRIM
Asunto principal:
Farmacología
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ARN Mensajero
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Línea Celular
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Apoptosis
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Proteínas Proto-Oncogénicas c-bcl-2
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Xantonas
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Proteína X Asociada a bcl-2
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Citometría de Flujo
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Genética
Límite:
Humans
Idioma:
Zh
Revista:
Journal of Experimental Hematology
Año:
2009
Tipo del documento:
Article