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Article: A small dose of hydrogen peroxide enhances tumor necrosis factor-alpha toxicity in inducing human vascular endothelial cell apoptosis: Reversal with propofol

TitleA small dose of hydrogen peroxide enhances tumor necrosis factor-alpha toxicity in inducing human vascular endothelial cell apoptosis: Reversal with propofol
Authors
Issue Date2006
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
Citation
Anesthesia And Analgesia, 2006, v. 103 n. 1, p. 110-116 How to Cite?
AbstractWe designed the present study to test the hypothesis that oxygen free radicals can enhance tumor necrosis factor (TNF)-α cellular toxicity, which might be reversed by propofol, an anesthetic with antioxidant properties, in human vascular endothelial cell line ECV304. Cultured ECV304 were either not treated, treated with 10 μM of hydrogen peroxide (H 2O 2), treated with TNF-α (40 ng/mL) alone, TNF-α in the presence of 10 μM of H 2O 2 (H+T), or propofol plus H 2O 2 for 24 h. Cell viability was measured by lactate dehydrogenate (LDH) assay. Cell apoptosis was assessed by flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end-labeling. The antiapoptotic Bcl-2 and pro-apoptotic Bax protein expressions were measured by immunocytochemical analysis. Increases in apoptosis, Bax, lipid peroxidation product malondialdehyde, LDH, and decreases in Bcl-2, superoxide dismutase, and glutathione peroxidase were observed in TNF-α-treated cells. H 2O 2 10 μM did not cause significant lipid peroxidation (0.75 ± 0.03 nmol/mg of malondialdehyde protein) as compared with control (0.70 ± 0.04 nmol/mg of malondialdehyde protein) (P > 0.05) but further enhanced TNF-α-induced lipid peroxidation, upregulated Bax, and down-regulated Bcl-2 expression and enhanced TNF-α-induced cell apoptosis (P < 0.05). Propofol 50 μM attenuated TNF-α and H 2O 2-induced cell apoptosis, accompanied by decreases in malondialdehyde and LDH production and restoration of Bcl-2 expression. Propofol exerts protective effects against H 2O 2-enhanced TNF-α cell toxicity by reducing oxidative injury. Copyright © 2006 International Anesthesia Research Society.
Persistent Identifierhttp://hdl.handle.net/10722/147231
ISSN
2015 Impact Factor: 3.827
2015 SCImago Journal Rankings: 1.523
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLuo, Ten_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.citationAnesthesia And Analgesia, 2006, v. 103 n. 1, p. 110-116en_US
dc.identifier.issn0003-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/147231-
dc.description.abstractWe designed the present study to test the hypothesis that oxygen free radicals can enhance tumor necrosis factor (TNF)-α cellular toxicity, which might be reversed by propofol, an anesthetic with antioxidant properties, in human vascular endothelial cell line ECV304. Cultured ECV304 were either not treated, treated with 10 μM of hydrogen peroxide (H 2O 2), treated with TNF-α (40 ng/mL) alone, TNF-α in the presence of 10 μM of H 2O 2 (H+T), or propofol plus H 2O 2 for 24 h. Cell viability was measured by lactate dehydrogenate (LDH) assay. Cell apoptosis was assessed by flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end-labeling. The antiapoptotic Bcl-2 and pro-apoptotic Bax protein expressions were measured by immunocytochemical analysis. Increases in apoptosis, Bax, lipid peroxidation product malondialdehyde, LDH, and decreases in Bcl-2, superoxide dismutase, and glutathione peroxidase were observed in TNF-α-treated cells. H 2O 2 10 μM did not cause significant lipid peroxidation (0.75 ± 0.03 nmol/mg of malondialdehyde protein) as compared with control (0.70 ± 0.04 nmol/mg of malondialdehyde protein) (P > 0.05) but further enhanced TNF-α-induced lipid peroxidation, upregulated Bax, and down-regulated Bcl-2 expression and enhanced TNF-α-induced cell apoptosis (P < 0.05). Propofol 50 μM attenuated TNF-α and H 2O 2-induced cell apoptosis, accompanied by decreases in malondialdehyde and LDH production and restoration of Bcl-2 expression. Propofol exerts protective effects against H 2O 2-enhanced TNF-α cell toxicity by reducing oxidative injury. Copyright © 2006 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.meshCells, Cultureden_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelial Cells - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshFree Radical Scavengers - Pharmacologyen_US
dc.subject.meshGlutathione Peroxidase - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshHydrogen Peroxide - Pharmacologyen_US
dc.subject.meshIn Situ Nick-End Labelingen_US
dc.subject.meshL-Lactate Dehydrogenase - Metabolismen_US
dc.subject.meshLipid Peroxidationen_US
dc.subject.meshMalondialdehyde - Metabolismen_US
dc.subject.meshPropofol - Pharmacologyen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Metabolismen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Toxicityen_US
dc.subject.meshBcl-2-Associated X Protein - Metabolismen_US
dc.titleA small dose of hydrogen peroxide enhances tumor necrosis factor-alpha toxicity in inducing human vascular endothelial cell apoptosis: Reversal with propofolen_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.0000221183.02244.80en_US
dc.identifier.pmid16790636en_US
dc.identifier.scopuseid_2-s2.0-33745815354en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745815354&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume103en_US
dc.identifier.issue1en_US
dc.identifier.spage110en_US
dc.identifier.epage116en_US
dc.identifier.isiWOS:000238661900022-
dc.publisher.placeUnited Statesen_US

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