نمایش پرونده ساده آیتم

dc.contributor.authorNezami, N
dc.contributor.authorGhorbanihaghjo, A
dc.contributor.authorArgani, H
dc.contributor.authorSafa, J
dc.contributor.authorRashtchizadeh, N
dc.contributor.authorVatankhah, AM
dc.contributor.authorSalari, B
dc.contributor.authorHajhosseini, B
dc.date.accessioned2018-08-26T08:08:51Z
dc.date.available2018-08-26T08:08:51Z
dc.date.issued2011
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/50382
dc.description.abstractObjectives: To investigate the effect of lovastatin therapy and withdrawal on paraoxonase 1 (PON1) and arylesterase (ARE) activities, and low-density lipoprotein cholesterol (LDL-C) susceptibility to oxidation in people with type 2 diabetic nephropathy (T2DN). Design and methods: Lovastatin (20 mg/day) was administered to 30 people with T2DN for 90 days and then withdrawn for 30 days. PON1 and ARE activities were measured by the spectrophotometric method. Susceptibility of LDL-C to oxidation was determined as the production of conjugated dienes. Results: After 90 days of lovastatin intervention, PON1 and ARE activities and LDL-C lag phase were significantly increased (p = 0.004, 0.002, and <0.001), while after 30 days of lovastatin withdrawal, PON1 and ARE activities and LDL-C lag phase had not changed significantly. Conclusion: Lovastatin therapy improves PON1 and ARE activities, and LDL-C susceptibility to oxidation. Despite withdrawal of lovastatin, PON1 and ARE activities, and LDL-C susceptibility to oxidation remain unchanged in people with T2DN. (C) 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
dc.language.isoEnglish
dc.relation.ispartofCLINICAL BIOCHEMISTRY
dc.subjectDiabetes
dc.subjectNephropathy
dc.subjectLipid peroxidation
dc.subjectArylesterase
dc.subjectLovastatin
dc.subjectHMG-CoA reductase inhibitors
dc.titleLovastatin enhances paraoxonase enzyme activity and quells low-density lipoprotein susceptibility to oxidation in type 2 diabetic nephropathy
dc.typeArticle
dc.citation.volume44
dc.citation.issue2-3
dc.citation.spage165
dc.citation.epage170
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1016/j.clinbiochem.2010.10.006


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