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Article: Dioscin (saponin)-induced generation of reactive oxygen species through mitochondria dysfunction: A proteomic-based study

TitleDioscin (saponin)-induced generation of reactive oxygen species through mitochondria dysfunction: A proteomic-based study
Authors
KeywordsAnticancer drug
Apoptosis
Dioscin
Mitochondria
Reactive oxygen species
Issue Date2007
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobs
Citation
Journal Of Proteome Research, 2007, v. 6 n. 12, p. 4703-4710 How to Cite?
AbstractIt is generally believed that traditional Chinese medicine such as saponins has great value as potent cancer prevention and chemotherapeutic agents; however, the molecular basis for their activities is for the most part lacking. In the present study, we used proteomics to examine the cytotoxic effect of dioscin, a glucoside saponin, on human myeloblast leukemia HL-60 cells. Dioscin induced apoptosis in HL-60 cells in a time-dependent manner. Protein profiling of the microsomal fraction with enriched plasma membrane proteins isolated from HL-60 cells revealed that proteins act as chaperones and/or mediators of protein folding and were substantially altered in expression cells upon dioscin stimuli. Further biochemical study indicated that mitochondria dysfunction caused generation of reactive oxygen species (ROS), leading to the changes in protein expression. The mitochondrial transmembrane potential (ΔΨm) inhibitor aristolochic acid (ArA) partially abrogated the dioscin-initiated death receptor apoptosis pathway and cell death. The current study provided detailed evidence to support that dioscin is capable of inducing apoptosis in mammalian cells, in which the mitochondria-initiated apoptosis pathway plays an important role. © 2007 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/69336
ISSN
2015 Impact Factor: 4.173
2015 SCImago Journal Rankings: 1.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorChiu, JFen_HK
dc.contributor.authorHe, QYen_HK
dc.date.accessioned2010-09-06T06:12:43Z-
dc.date.available2010-09-06T06:12:43Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Proteome Research, 2007, v. 6 n. 12, p. 4703-4710en_HK
dc.identifier.issn1535-3893en_HK
dc.identifier.urihttp://hdl.handle.net/10722/69336-
dc.description.abstractIt is generally believed that traditional Chinese medicine such as saponins has great value as potent cancer prevention and chemotherapeutic agents; however, the molecular basis for their activities is for the most part lacking. In the present study, we used proteomics to examine the cytotoxic effect of dioscin, a glucoside saponin, on human myeloblast leukemia HL-60 cells. Dioscin induced apoptosis in HL-60 cells in a time-dependent manner. Protein profiling of the microsomal fraction with enriched plasma membrane proteins isolated from HL-60 cells revealed that proteins act as chaperones and/or mediators of protein folding and were substantially altered in expression cells upon dioscin stimuli. Further biochemical study indicated that mitochondria dysfunction caused generation of reactive oxygen species (ROS), leading to the changes in protein expression. The mitochondrial transmembrane potential (ΔΨm) inhibitor aristolochic acid (ArA) partially abrogated the dioscin-initiated death receptor apoptosis pathway and cell death. The current study provided detailed evidence to support that dioscin is capable of inducing apoptosis in mammalian cells, in which the mitochondria-initiated apoptosis pathway plays an important role. © 2007 American Chemical Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobsen_HK
dc.relation.ispartofJournal of Proteome Researchen_HK
dc.subjectAnticancer drugen_HK
dc.subjectApoptosisen_HK
dc.subjectDioscinen_HK
dc.subjectMitochondriaen_HK
dc.subjectReactive oxygen speciesen_HK
dc.titleDioscin (saponin)-induced generation of reactive oxygen species through mitochondria dysfunction: A proteomic-based studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-3893&volume=6&spage=4703&epage=4710&date=2007&atitle=Dioscin+(Saponin)-induced+generation+of+reactive+oxygen+species+through+mitochondria+dysfunction:+A+proteomic-based+studyen_HK
dc.identifier.emailChe, CM:cmche@hku.hken_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1021/pr070399ren_HK
dc.identifier.pmid17975908-
dc.identifier.scopuseid_2-s2.0-38049075602en_HK
dc.identifier.hkuros141557en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38049075602&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue12en_HK
dc.identifier.spage4703en_HK
dc.identifier.epage4710en_HK
dc.identifier.isiWOS:000251546200019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=7601490707en_HK
dc.identifier.scopusauthoridChe, CM=7102442791en_HK
dc.identifier.scopusauthoridChiu, JF=7201501692en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK

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