Atorvastatin preferentially reduces LDL-associated platelet-activating factor acetylhydrolase activity in dyslipidemias of type IIA and type IIB

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dc.contributor.authorTsimihodimos, V.en
dc.contributor.authorKarabina, S. A. P.en
dc.contributor.authorTambaki, A. P.en
dc.contributor.authorBairaktari, E.en
dc.contributor.authorGoudevenos, J. A.en
dc.contributor.authorChapman, M. J.en
dc.contributor.authorElisaf, M.en
dc.contributor.authorTselepis, A. D.en
dc.date.accessioned2015-11-24T16:52:55Z
dc.date.available2015-11-24T16:52:55Z
dc.identifier.issn1079-5642-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/9943
dc.rightsDefault Licence-
dc.subjecthyperlipidemiaen
dc.subjectmonocytes/macrophagesen
dc.subjectplatelet-activating factor acetylhydrolaseen
dc.subjectparaoxonaseen
dc.subjectatorvastatinen
dc.subjectlow-density-lipoproteinen
dc.subjectdependent diabetes-mellitusen
dc.subjecthuman-plasmaen
dc.subjectfamilial hypercholesterolemiaen
dc.subjectparaoxonase activityen
dc.subjectpaf-acetylhydrolaseen
dc.subjectphospholipase a(2)en
dc.subjectcoronary hearten
dc.subjectoxidationen
dc.subjecttherapyen
dc.titleAtorvastatin preferentially reduces LDL-associated platelet-activating factor acetylhydrolase activity in dyslipidemias of type IIA and type IIBen
heal.abstractHuman plasma platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A(2) that is primarily associated with low density lipoprotein (LDL). PAF-AH activity has also been found in high density lipoprotein (HDL), although it has recently been indicated that there is no PAF-AH protein in HDL. Plasma paraoxonase 1 (PON1) is an HDL-associated esterase, which also exhibits PAF-AH-like activity. The effect of atorvastatin (20 mg per day for 4 months) on PAF-AH and PON1 activities in patients with dyslipidemia of type IIA (n=55) or type IIB (n=21) was studied. In both patient groups, atorvastatin significantly reduced plasma PAF-AH activity because of the decrease in LDL plasma levels and the preferential decrease in PAF-AH activity on dense LDL subfractions (LDL-4 and LDL-5). Drug therapy did not affect HDL-associated PAF-AH activity or serum PON1 activities toward paraoxon and phenylacetate in either patient group. However, because of the reduction in LDL cholesterol levels, the ratios of HDL-associated PAF-AH and serum PON1 activities to LDL cholesterol levels were significantly increased after drug administration. The reduction of the LDL-associated PAF-AH activity and the elevation in the ratios of HDL-associated PAF-AH and PON1 activities to LDL plasma levels may represent a new dimension in the antiatherogenic effect of atorvastatin.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondary<Go to ISI>://000173786600017-
heal.identifier.secondaryhttp://atvb.ahajournals.org/content/22/2/306.full.pdf-
heal.journalNameArteriosclerosis Thrombosis and Vascular Biologyen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate2002-
heal.publisherAmerican Heart Association, Inc.en
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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