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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

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
Authors
Issue Date2005
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
Citation
Anesthesia And Analgesia, 2005, v. 100 n. 6, p. 1653-1659 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/147211
ISSN
2014 Impact Factor: 3.472
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLuo, Ten_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorAnsley, DMen_US
dc.contributor.authorOuyang, Jen_US
dc.contributor.authorGranville, DJen_US
dc.contributor.authorLi, Yen_US
dc.contributor.authorXia, ZYen_US
dc.contributor.authorZhou, QSen_US
dc.contributor.authorLiu, XYen_US
dc.date.accessioned2012-05-29T06:00:49Z-
dc.date.available2012-05-29T06:00:49Z-
dc.date.issued2005en_US
dc.identifier.citationAnesthesia And Analgesia, 2005, v. 100 n. 6, p. 1653-1659en_US
dc.identifier.issn0003-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/147211-
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.en_US
dc.languageengen_US
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.orgen_US
dc.relation.ispartofAnesthesia and Analgesiaen_US
dc.subject.meshAnesthetics, Intravenous - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelial Cells - Drug Effects - Ultrastructureen_US
dc.subject.meshGenes, Bcl-2 - Genetics - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Nick-End Labelingen_US
dc.subject.meshNitric Oxide - Biosynthesis - Physiologyen_US
dc.subject.meshPropofol - Pharmacologyen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Genetics - Physiologyen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshUmbilical Veins - Cytology - Drug Effectsen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
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 generationen_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.doi10.1213/01.ANE.0000150945.95254.D8en_US
dc.identifier.pmid15920191en_US
dc.identifier.scopuseid_2-s2.0-19044379949en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19044379949&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume100en_US
dc.identifier.issue6en_US
dc.identifier.spage1653en_US
dc.identifier.epage1659en_US
dc.identifier.isiWOS:000229305600018-
dc.publisher.placeUnited Statesen_US

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