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Conference Paper: Nitroglycerin reduces TNF-alpha toxicity to endothelial cells but compromises the protective effects of propofol

TitleNitroglycerin reduces TNF-alpha toxicity to endothelial cells but compromises the protective effects of propofol
Authors
KeywordsBiology
Issue Date2010
PublisherFederation of American Societies for Experimental Biology.
Citation
Experiment Biology Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 959 How to Cite?
AbstractSupplementation of nitroglycerin (NTG) may increase cardiomyocyte death during ischemia (Histol Histopathol 2009;24(12):1487–98) and the underlying mechanism is unknown. Vascular endothelial cell apoptosis precedes cardiomyocyte apoptosis during myocardial ischemia-reperfusion, a situation that is associated with increased tumor necrosis factor-α (TNF) production. We postulated that NTG may exacerbate TNF induced endothelial cell apoptosis by enhancing nitrative stress. Cultured human umbilical vein endothelial cells were either not treated (control), treated with TNF (40 ng/ml) alone or TNF in the presence of NTG, propofol (an anesthetic that scavenges peroxynitrite), or NTG plus propofol, respectively, for 16 hr. TNF increased endothelial cell apoptosis, accompanied by increased protein expression of nitrotyrosine, a footprint of peroxynitrite and an index of nitrative stress. Both NTG and propofol attenuated TNF-induced cell apoptosis, however this protective effect diminished when NTG and propofol were used in combination and this was accompanied by increased nitrotyrosine expression and protein kinase C-β2 phosphorylation at site ser660. NTG may have compromised propofol cellular protection by counteracting its peroxynitrite scavenging capacity.
Persistent Identifierhttp://hdl.handle.net/10722/126898
ISSN
2014 Impact Factor: 5.043
2014 SCImago Journal Rankings: 2.516

 

DC FieldValueLanguage
dc.contributor.authorLiu, HMen_HK
dc.contributor.authorLei, Sen_HK
dc.contributor.authorLuo, Ten_HK
dc.contributor.authorXia, ZYen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorXia, Zen_HK
dc.date.accessioned2010-10-31T12:54:57Z-
dc.date.available2010-10-31T12:54:57Z-
dc.date.issued2010en_HK
dc.identifier.citationExperiment Biology Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 959en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/126898-
dc.description.abstractSupplementation of nitroglycerin (NTG) may increase cardiomyocyte death during ischemia (Histol Histopathol 2009;24(12):1487–98) and the underlying mechanism is unknown. Vascular endothelial cell apoptosis precedes cardiomyocyte apoptosis during myocardial ischemia-reperfusion, a situation that is associated with increased tumor necrosis factor-α (TNF) production. We postulated that NTG may exacerbate TNF induced endothelial cell apoptosis by enhancing nitrative stress. Cultured human umbilical vein endothelial cells were either not treated (control), treated with TNF (40 ng/ml) alone or TNF in the presence of NTG, propofol (an anesthetic that scavenges peroxynitrite), or NTG plus propofol, respectively, for 16 hr. TNF increased endothelial cell apoptosis, accompanied by increased protein expression of nitrotyrosine, a footprint of peroxynitrite and an index of nitrative stress. Both NTG and propofol attenuated TNF-induced cell apoptosis, however this protective effect diminished when NTG and propofol were used in combination and this was accompanied by increased nitrotyrosine expression and protein kinase C-β2 phosphorylation at site ser660. NTG may have compromised propofol cellular protection by counteracting its peroxynitrite scavenging capacity.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology.-
dc.relation.ispartofThe FASEB Journalen_HK
dc.subjectBiology-
dc.titleNitroglycerin reduces TNF-alpha toxicity to endothelial cells but compromises the protective effects of propofolen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLiu, HM: huimin_liu2006@126.comen_HK
dc.identifier.emailLei, S: leishaoqing@163.comen_HK
dc.identifier.emailLeung, GPH: leung_pak_heng@hotmail.comen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_HK
dc.identifier.emailXia, Z: zhengyuan_xia@yahoo.comen_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros171206en_HK
dc.identifier.volume24en_HK
dc.identifier.issueMeeting abstract suppl.-
dc.description.otherExperiment Biology Meeting (EB 2010), Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 959-
dc.description.otherOpen Access Journal-

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