Troglitazone induced apoptosis via PPARγ activated POX-induced ROS formation in HT29 cells / 生物医学与环境科学(英文)
Biomedical and Environmental Sciences
; (12): 391-399, 2011.
Article
em En
| WPRIM
| ID: wpr-306847
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>In order to investigate the potential mechanisms in troglitazone-induced apoptosis in HT29 cells, the effects of PPARγ and POX-induced ROS were explored.</p><p><b>METHODS</b>[3- (4, 5)-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay, Annexin V and PI staining using FACS, plasmid transfection, ROS formation detected by DCFH staining, RNA interference, RT-PCR & RT-QPCR, and Western blotting analyses were employed to investigate the apoptotic effect of troglitazone and the potential role of PPARγ pathway and POX-induced ROS formation in HT29 cells.</p><p><b>RESULTS</b>Troglitazone was found to inhibit the growth of HT29 cells by induction of apoptosis. During this process, mitochondria related pathways including ROS formation, POX expression and cytochrome c release increased, which were inhibited by pretreatment with GW9662, a specific antagonist of PPARγ. These results illustrated that POX upregulation and ROS formation in apoptosis induced by troglitazone was modulated in PPARγ-dependent pattern. Furthermore, the inhibition of ROS and apoptosis after POX siRNA used in troglitazone-treated HT29 cells indicated that POX be essential in the ROS formation and PPARγ-dependent apoptosis induced by troglitazone.</p><p><b>CONCLUSION</b>The findings from this study showed that troglitazone-induced apoptosis was mediated by POX-induced ROS formation, at least partly, via PPARγ activation.</p>
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Assunto principal:
Farmacologia
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Prolina Oxidase
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Regulação Neoplásica da Expressão Gênica
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Cromanos
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Espécies Reativas de Oxigênio
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Apoptose
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Células HT29
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Tiazolidinedionas
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Citocromos c
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PPAR gama
Limite:
Humans
Idioma:
En
Revista:
Biomedical and Environmental Sciences
Ano de publicação:
2011
Tipo de documento:
Article