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Article: Protective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis
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TitleProtective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis
 
AuthorsWang, F1
Xia, Z1
Luo, T1
Ouyang, J2
Xia, Z
 
KeywordsApoptosis
Endothelium
Hydrogen Peroxide
Propofol
Tumor Necrosis Factor-Alpha
 
Issue Date2006
 
CitationMedical 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.
 
ISSN1671-8852
2013 SCImago Journal Rankings: 0.100
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWang, F
 
dc.contributor.authorXia, Z
 
dc.contributor.authorLuo, T
 
dc.contributor.authorOuyang, J
 
dc.contributor.authorXia, Z
 
dc.date.accessioned2012-05-29T06:00:56Z
 
dc.date.available2012-05-29T06:00:56Z
 
dc.date.issued2006
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationMedical Journal Of Wuhan University, 2006, v. 27 n. 3, p. 338-341 [How to Cite?]
 
dc.identifier.epage341
 
dc.identifier.issn1671-8852
2013 SCImago Journal Rankings: 0.100
 
dc.identifier.issue3
 
dc.identifier.scopuseid_2-s2.0-33746359947
 
dc.identifier.spage338
 
dc.identifier.urihttp://hdl.handle.net/10722/147232
 
dc.identifier.volume27
 
dc.languageeng
 
dc.relation.ispartofMedical Journal of Wuhan University
 
dc.relation.referencesReferences in Scopus
 
dc.subjectApoptosis
 
dc.subjectEndothelium
 
dc.subjectHydrogen Peroxide
 
dc.subjectPropofol
 
dc.subjectTumor Necrosis Factor-Alpha
 
dc.titleProtective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis
 
dc.typeArticle
 
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<item><contributor.author>Wang, F</contributor.author>
<contributor.author>Xia, Z</contributor.author>
<contributor.author>Luo, T</contributor.author>
<contributor.author>Ouyang, J</contributor.author>
<contributor.author>Xia, Z</contributor.author>
<date.accessioned>2012-05-29T06:00:56Z</date.accessioned>
<date.available>2012-05-29T06:00:56Z</date.available>
<date.issued>2006</date.issued>
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<description.abstract>Objective: To test the hypothesis that oxygen free radicals can potentiate TNF-&#945; 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 &#956;mol/L hydrogen peroxide (H 2O 2) and treated with 40 nmol/L TNF-&#945; 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 &#956;mol/L, did not cause significant lipid peroxidation, but enhanced TNF-&#945; induced cell apoptosis (P&lt;0.01). Propofol at 50 &#956;mol/L attenuated TNF-&#945; 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-&#945; induced endothelial cell apoptosis. Propofol exerts protective effects against H 2O 2 potentiated TNF-&#945; cell toxicity by reduction of oxidative injury.</description.abstract>
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<subject>Apoptosis</subject>
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<subject>Tumor Necrosis Factor-Alpha</subject>
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Author Affiliations
  1. Hubei General Hospital
  2. Wuhan University