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Article: Propofol dose-dependently reduces tumor necrosis factor-α-induced human umbilical vein endothelial cell apoptosis: Effects on Bcl-2 and bax expression and nitric oxide generation
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TitlePropofol dose-dependently reduces tumor necrosis factor-α-induced human umbilical vein endothelial cell apoptosis: Effects on Bcl-2 and bax expression and nitric oxide generation
 
AuthorsLuo, T1
Xia, Z1 2 2
Ansley, DM2
Ouyang, J1
Granville, DJ2
Li, Y1
Xia, ZY1
Zhou, QS1
Liu, XY1
 
Issue Date2005
 
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
 
CitationAnesthesia And Analgesia, 2005, v. 100 n. 6, p. 1653-1659 [How to Cite?]
DOI: http://dx.doi.org/10.1213/01.ANE.0000150945.95254.D8
 
AbstractWe investigated whether propofol can inhibit tumor necrosis factor (TNF)-α-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). Isolated HUVECs were cultured in Dulbecco's modified Eagle medium supplemented with 20% bovine calf serum. HUVECs in untreated and propofol control groups were cultured at 37°C for 24.5 h. HUVECs in the TNF treatment groups were initially cultured for 30 min in the presence of TNF or various concentrations of propofol, respectively, which were then cultured for 24 h with the addition of TNF at 40 ng/mL in the medium. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and confirmed by electron microscopy. The antiapoptotic Bcl-2 and proapoptotic Bax protein expressions were measured by immunocytochemical analysis. TNF stimulation resulted in a reduced Bcl-2/ Bax ratio and increased apoptotic index (AI: percentage of apoptotic cells) in HUVECs. Propofol, at concentrations ≥12 μM, significantly (P < 0.001) and dose-dependently attenuated TNF-induced increase in AI and decrease in Bcl-2/Bax ratio. This was accompanied by increases in nitric oxide production. There is an inverse correlation between the ratio of Bcl-2/Bax expression and AI (P = 0.0009). These results suggest that propofol, at clinical relevant concentrations, can reduce TNF-induced HUVEC apoptosis. ©2005 by the International Anesthesia Research Society.
 
ISSN0003-2999
2012 Impact Factor: 3.3
2012 SCImago Journal Rankings: 1.333
 
DOIhttp://dx.doi.org/10.1213/01.ANE.0000150945.95254.D8
 
ISI Accession Number IDWOS:000229305600018
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLuo, T
 
dc.contributor.authorXia, Z
 
dc.contributor.authorAnsley, DM
 
dc.contributor.authorOuyang, J
 
dc.contributor.authorGranville, DJ
 
dc.contributor.authorLi, Y
 
dc.contributor.authorXia, ZY
 
dc.contributor.authorZhou, QS
 
dc.contributor.authorLiu, XY
 
dc.date.accessioned2012-05-29T06:00:49Z
 
dc.date.available2012-05-29T06:00:49Z
 
dc.date.issued2005
 
dc.description.abstractWe investigated whether propofol can inhibit tumor necrosis factor (TNF)-α-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). Isolated HUVECs were cultured in Dulbecco's modified Eagle medium supplemented with 20% bovine calf serum. HUVECs in untreated and propofol control groups were cultured at 37°C for 24.5 h. HUVECs in the TNF treatment groups were initially cultured for 30 min in the presence of TNF or various concentrations of propofol, respectively, which were then cultured for 24 h with the addition of TNF at 40 ng/mL in the medium. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and confirmed by electron microscopy. The antiapoptotic Bcl-2 and proapoptotic Bax protein expressions were measured by immunocytochemical analysis. TNF stimulation resulted in a reduced Bcl-2/ Bax ratio and increased apoptotic index (AI: percentage of apoptotic cells) in HUVECs. Propofol, at concentrations ≥12 μM, significantly (P < 0.001) and dose-dependently attenuated TNF-induced increase in AI and decrease in Bcl-2/Bax ratio. This was accompanied by increases in nitric oxide production. There is an inverse correlation between the ratio of Bcl-2/Bax expression and AI (P = 0.0009). These results suggest that propofol, at clinical relevant concentrations, can reduce TNF-induced HUVEC apoptosis. ©2005 by the International Anesthesia Research Society.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAnesthesia And Analgesia, 2005, v. 100 n. 6, p. 1653-1659 [How to Cite?]
DOI: http://dx.doi.org/10.1213/01.ANE.0000150945.95254.D8
 
dc.identifier.doihttp://dx.doi.org/10.1213/01.ANE.0000150945.95254.D8
 
dc.identifier.epage1659
 
dc.identifier.isiWOS:000229305600018
 
dc.identifier.issn0003-2999
2012 Impact Factor: 3.3
2012 SCImago Journal Rankings: 1.333
 
dc.identifier.issue6
 
dc.identifier.pmid15920191
 
dc.identifier.scopuseid_2-s2.0-19044379949
 
dc.identifier.spage1653
 
dc.identifier.urihttp://hdl.handle.net/10722/147211
 
dc.identifier.volume100
 
dc.languageeng
 
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAnesthesia and Analgesia
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnesthetics, Intravenous - Pharmacology
 
dc.subject.meshApoptosis - Drug Effects
 
dc.subject.meshCell Survival - Drug Effects
 
dc.subject.meshCells, Cultured
 
dc.subject.meshDose-Response Relationship, Drug
 
dc.subject.meshEndothelial Cells - Drug Effects - Ultrastructure
 
dc.subject.meshGenes, Bcl-2 - Genetics - Physiology
 
dc.subject.meshHumans
 
dc.subject.meshIn Situ Nick-End Labeling
 
dc.subject.meshNitric Oxide - Biosynthesis - Physiology
 
dc.subject.meshPropofol - Pharmacology
 
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Genetics - Physiology
 
dc.subject.meshTumor Necrosis Factor-Alpha - Antagonists & Inhibitors - Pharmacology
 
dc.subject.meshUmbilical Veins - Cytology - Drug Effects
 
dc.subject.meshBcl-2-Associated X Protein
 
dc.titlePropofol dose-dependently reduces tumor necrosis factor-α-induced human umbilical vein endothelial cell apoptosis: Effects on Bcl-2 and bax expression and nitric oxide generation
 
dc.typeArticle
 
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Author Affiliations
  1. Wuhan University
  2. The University of British Columbia