Honokiol-induced apoptosis of human non-Hodgkin lymphoma Raji cells and its possible mechanism / 南方医科大学学报
Journal of Southern Medical University
;
(12): 1918-1921, 2011.
Artigo
em Chinês
| WPRIM
| ID: wpr-265752
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the apoptosis-inducing effect of honokiol on human non-Hodgkin lymphoma Raji cells and the possible mechanism.</p><p><b>METHODS</b>Raji cells were treated with different concentrations of honokiol, and the proliferation of the cells was detected using MTT assay. Flow cytometry was employed to analyze the cell cycle changes and apoptosis of honokiol-treated cells. Caspase 8 activity in the cells was measured by caspase 8 kit, and RT-PCR was used to detect the expression of apoptosis-related genes Bcl-2, Bad, and Bax.</p><p><b>RESULTS</b>Honokiol significantly inhibited the growth of Raji cells in a time- and dose-dependent manner, with IC(50) concentration of 17.53, 12.61, and 7.4 µg/ml at 12, 24, 48 h, respectively. Flow cytometry revealed cell cycle arrest at G0/G1 phase following honokiol treatment. The apoptosis rates of Raji cells treated with 7.5 and 15 µg/ml honokiol were significantly higher than that of the control cells [(18.24∓2.53)%, (28.44∓2.48)% vs (4.84∓1.15)%, P<0.01]. Caspase 8 activity in Raji cells was significantly enhanced by honokiol (P<0.05). The mRNA expression of the apoptosis-promoting gene Bad was significantly increased following honokiol treatment (P<0.01), while the expressions of Bcl-2 and Bax remained unchanged.</p><p><b>CONCLUSION</b>Honokiol can induce apoptosis in Raji cells possibly in relation to enhancement of caspase 8 activity and Bad gene expression.</p>
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Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Compostos de Bifenilo
/
Linfoma não Hodgkin
/
Linfoma de Burkitt
/
Apoptose
/
Lignanas
/
Linhagem Celular Tumoral
/
Proliferação de Células
/
Proteína de Morte Celular Associada a bcl
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2011
Tipo de documento:
Artigo
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