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Troglitazone Induced Apoptosis via PPARy Activated POX-induced ROS Formation in HT29 Cells

摘要Objective In order to investigate the potential mechanisms in troglitazone-induced apoptosis in HT29 cells,the effects of PPARY and POX-induced ROS were explored.Methods [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 PPARY pathway and POX-induced ROS formation in HT29 cells.Results 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 PPARY.These results illustrated that POX upregulation and ROS formation in apoptosis induced by troglitazone was modulated in PPARY-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 PPARy-dependent apoptosis induced by troglitazone.Conclusion The findings from this study showed that troglitazone-induced apoptosis was mediated by POX-induced ROS formation,at least partly,via PPARY activation.

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DOI 10.3967/0895-3988.2011.04.010
发布时间 2011-12-05(万方平台首次上网日期,不代表论文的发表时间)
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生物医学与环境科学(英文版)

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