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dc.contributor.authorOkuyucu, Ali
dc.contributor.authorSalis, Osman
dc.contributor.authorAlici, Omer
dc.contributor.authorIlkaya, Fatih
dc.contributor.authorAltuntas, Aynur
dc.contributor.authorGuvenli, Abdullah
dc.contributor.authorAlacam, Hasan
dc.date.accessioned2020-06-21T13:51:28Z
dc.date.available2020-06-21T13:51:28Z
dc.date.issued2015
dc.identifier.issn0393-6384
dc.identifier.issn2283-9720
dc.identifier.urihttps://hdl.handle.net/20.500.12712/14693
dc.descriptionWOS: 000357346000011en_US
dc.description.abstractIntroduction: The endothelium plays an important role in maintaining vascular structure and waits; and endothelial cells are protective against the thrombosis and atherosclerosis. Cardiovascular risk factors, such as metabolic diseases, systemic and local inflammations, result in endothelial dysfunction. Nitric oxide is one of the endothelium derived substances that has an important role in maintaining the endothelial homeostasis. The asymmetric dimethylarginine (ADMA) is the endogenous inhibitor of the nitric oxide synthase. ADMA has been shown to impair the endothelial function and to be associated with hypercholesterolemia, hyperhomocysteinemia, and atherosclerosis. Ascorbic acid, a vitamin with reductant and antioxidant effects, can improve endothelial function and decrease the reactive oxygen species level. Our objective was to determine pathologically exogenous ADMA effect on endothelium of abdominal aorta, and to observe protective effect of antioxidant ascorbic acid. Materials and methods: The rats were divided in three groups: control, ADMA and ADMA + ascorbic acid. After administration of ADMA and ascorbic acid for 10 days, the blood was collected and abdominal aorta removed from the animals. Homocysteine, triglyceride, and cholesterol levels were measured by autoanalyzer. Abdominal aorta was evaluated histopathologically and the intimal thickness was measured using an imaging system. Result: The ADMA increased the intimal thickness (p=0.003), and ascorbic acid inhibited this increase (p=0.001). ADMA also increased the levels of triglyceride and cholesterol (p=0.008 and p=0.001), and the increased triglyceride and cholesterol levels are inhibited by ascorbic acid (p=0.000 and p=0.00I). Conclusions: Increased intimal thickness by delivering exogenous ADMA supports that exogenous ADMA might be one of the factors resulting in atherosclerosis. We consider that the increase in intima thickness may not be a direct effect of ADMA but may be secondary to the increased cholesterol levels and ascorbic acid can be protective for atherosclerosis.en_US
dc.language.isoengen_US
dc.publisherCarbone Editoreen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAsymmetric dimethylarginineen_US
dc.subjectcholesterolen_US
dc.subjectintimal thicknessen_US
dc.subjectascorbic aciden_US
dc.titleThe Protective Effect of Ascorbic Acid on Exogenous Asymmetric Dimethylarginine Induced Intimal Thickness and Cholesterol Increase in Ratsen_US
dc.typearticleen_US
dc.contributor.departmentOMÜen_US
dc.identifier.volume31en_US
dc.identifier.issue4en_US
dc.identifier.startpage835en_US
dc.identifier.endpage840en_US
dc.relation.journalActa Medica Mediterraneaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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