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Article: Protective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis

TitleProtective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis
Authors
KeywordsApoptosis
Endothelium
Hydrogen Peroxide
Propofol
Tumor Necrosis Factor-Alpha
Issue Date2006
Citation
Medical Journal Of Wuhan University, 2006, v. 27 n. 3, p. 338-341 How to Cite?
AbstractObjective: To test the hypothesis that oxygen free radicals can potentiate TNF-α cellular toxicity, which might be reserved by propofol in human vascular endothelial cells. Methods: Cultured human ECV304 cells were divided into five groups: untreated (Control), treated with 10 μmol/L hydrogen peroxide (H 2O 2) and treated with 40 nmol/L TNF-α alone (T) or in the presence of H 2O 2 (T+H) or in propofol + H 2O 2 (T+H+P), with each cultured for 24 hours. Cell apoptosis was assessed by flow cytometry. The concentration of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected at the same time. Results: H 2O 2, at 10 μmol/L, did not cause significant lipid peroxidation, but enhanced TNF-α induced cell apoptosis (P<0.01). Propofol at 50 μmol/L attenuated TNF-α and H 2O 2 induced cell apoptosis, accompanied with a decrease in MDA, while with increases in SOD and GSH-Px. Conclusion: H 2O 2, even at trace concentration, may significantly enhance TNF-α induced endothelial cell apoptosis. Propofol exerts protective effects against H 2O 2 potentiated TNF-α cell toxicity by reduction of oxidative injury.
Persistent Identifierhttp://hdl.handle.net/10722/147232
ISSN
2014 SCImago Journal Rankings: 0.100
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Fen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorLuo, Ten_US
dc.contributor.authorOuyang, Jen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:00:56Z-
dc.date.available2012-05-29T06:00:56Z-
dc.date.issued2006en_US
dc.identifier.citationMedical Journal Of Wuhan University, 2006, v. 27 n. 3, p. 338-341en_US
dc.identifier.issn1671-8852en_US
dc.identifier.urihttp://hdl.handle.net/10722/147232-
dc.description.abstractObjective: To test the hypothesis that oxygen free radicals can potentiate TNF-α cellular toxicity, which might be reserved by propofol in human vascular endothelial cells. Methods: Cultured human ECV304 cells were divided into five groups: untreated (Control), treated with 10 μmol/L hydrogen peroxide (H 2O 2) and treated with 40 nmol/L TNF-α alone (T) or in the presence of H 2O 2 (T+H) or in propofol + H 2O 2 (T+H+P), with each cultured for 24 hours. Cell apoptosis was assessed by flow cytometry. The concentration of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected at the same time. Results: H 2O 2, at 10 μmol/L, did not cause significant lipid peroxidation, but enhanced TNF-α induced cell apoptosis (P<0.01). Propofol at 50 μmol/L attenuated TNF-α and H 2O 2 induced cell apoptosis, accompanied with a decrease in MDA, while with increases in SOD and GSH-Px. Conclusion: H 2O 2, even at trace concentration, may significantly enhance TNF-α induced endothelial cell apoptosis. Propofol exerts protective effects against H 2O 2 potentiated TNF-α cell toxicity by reduction of oxidative injury.en_US
dc.languageengen_US
dc.relation.ispartofMedical Journal of Wuhan Universityen_US
dc.subjectApoptosisen_US
dc.subjectEndotheliumen_US
dc.subjectHydrogen Peroxideen_US
dc.subjectPropofolen_US
dc.subjectTumor Necrosis Factor-Alphaen_US
dc.titleProtective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosisen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33746359947en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746359947&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue3en_US
dc.identifier.spage338en_US
dc.identifier.epage341en_US

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