Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/68523
DC FieldValueLanguage
dc.contributor.authorSheu, M.J.en_US
dc.contributor.authorChou, P.Y.en_US
dc.contributor.authorHuang, C.S.en_US
dc.contributor.authorTsai, I.C.en_US
dc.contributor.authorChien, Y.C.en_US
dc.contributor.authorLin, S.Y.en_US
dc.contributor.authorTsai, H.Y.en_US
dc.contributor.authorCheng, H.C.en_US
dc.contributor.authorWu, C.H.en_US
dc.date2010zh_TW
dc.date.accessioned2014-06-11T05:56:56Z-
dc.date.available2014-06-11T05:56:56Z-
dc.identifier.issn0305-1870zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/68523-
dc.description.abstractP>1. The aim of the present study was to investigate the molecular mechanisms by which pipoxolan exerts its inhibitory effects and apoptotic activity in human leukaemia HL-60 cells. 2. The effects of pipoxolan on the proliferation of HL-60 cells and on the distribution of cells within different phases of the cell cycle were investigated indirectly using a Trypan blue assay and a flow cytometer, respectively. The effects of pipoxolan on the apoptosis of HL-60 cells was investigated using DNA fragmentation and flow cytometer. The expression of factors affecting the cell cycle and apoptosis, including p53, p21, Bax, Bcl2, cytochrome c, caspase 3 and caspase 9, was examined by western blotting. 3. At 6.25 mu g/mL, pipoxolan significantly induced apoptosis in human leukaemia HL-60 cells after 24 h exposure. In addition, HL-60 cells were arrested in the G(0)/G(1) phase via the induction of p53/p21 by pipoxolan. Apoptosis was associated with an increased Bax/Bcl-2 ratio, cytochrome c release, cleavage of procaspases-9 and -3 and hydrolysis of poly(ADP-ribose) polymerase. Intracellular reactive oxygen species (ROS) seem to play a key role in the pipoxolan-induced apoptosis, because high levels of ROS were produced early in the drug treatment. Apoptosis was significantly abrogated by the free radical scavenger N-acetylcysteine (NAC).en_US
dc.language.isoen_USzh_TW
dc.relationClinical and Experimental Pharmacology and Physiologyen_US
dc.relation.ispartofseriesClinical and Experimental Pharmacology and Physiology, Volume 37, Issue 5-6, Page(s) 605-612.en_US
dc.relation.urihttp://dx.doi.org/10.1111/j.1440-1681.2010.05358.xen_US
dc.subjectanti-proliferationen_US
dc.subjectapoptosisen_US
dc.subjectcaspase 3en_US
dc.subjectpipoxolanen_US
dc.subjectreactive oxygenen_US
dc.subjectspeciesen_US
dc.subjectoxidative stressen_US
dc.subjectdna damageen_US
dc.subjectapoptosisen_US
dc.subjectdeathen_US
dc.subjectactivationen_US
dc.subjecttargeten_US
dc.subjectidentificationen_US
dc.subjectstimulationen_US
dc.subjectmechanismsen_US
dc.subjectpathwaysen_US
dc.titlePipoxolan inhibits proliferation of HL-60 human leukaemia cancer cells by arresting the cell cycle at the G(0)/G(1) phaseen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1111/j.1440-1681.2010.05358.xzh_TW
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en_US-
item.fulltextno fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
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