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dc.contributor.authorCayci, C.en_US
dc.contributor.authorWahlquist, T. C.en_US
dc.contributor.authorSeckin, S. I.en_US
dc.contributor.authorOzcan, V.en_US
dc.contributor.authorTekinay, A. B.en_US
dc.contributor.authorMartens, T. P.en_US
dc.contributor.authorOz, M. C.en_US
dc.contributor.authorAscherman, J. A.en_US
dc.date.accessioned2016-02-08T10:00:46Z
dc.date.available2016-02-08T10:00:46Z
dc.date.issued2010en_US
dc.identifier.issn0148-7043
dc.identifier.urihttp://hdl.handle.net/11693/22486
dc.description.abstractVessels respond to injury by a healing process that includes the development of neointima. Stenosis secondary to neointima formation is the main cause of failure following arterial reconstructions. Vessel wall homeostasis is regulated by proinflammatory cytokines that affect smooth muscle cell proliferation, growth, migration, and death. We assessed the hypothesis that naringenin, a flavinoid possessing anti-inflammatory, antioxidant, and antiproliferative activities, reduces neointimal hyperplasia (NIH) following vascular injury.Arterial injury was created by interposition grafting of autologous right superficial epigastric vein graft into the right femoral artery (FA) in 48 male Sprague-Dawley rats. Following injury, the rats were divided into 4 groups (n = 12). Two groups were treated with naringenin (100 mg/kg intraperitoneal q daily) for 2 and 4 weeks each while 2 control groups received normal saline for the same durations. For Sham group (n = 10), the FA and vein were isolated without any additional procedure. Rats were killed at the end of treatment regimen in all groups, and FAs were harvested. Thickness of intima was measured in histologic sections, and levels of platelet derived growth factor (PDGF)-BB, TNFα, and Ki67 labeling index (Ki67 LI) were quantified in immunohistochemical analyses to assess the amount of NIH and mechanisms underlying its formation.Although there was no significant difference between the groups at 2 weeks, neointima thickness was lower in the naringenin treated group at 4 weeks (23.7 ± 2.3 vs. 35.6 ± 2.6 μm in control group; P < 0.001). The levels of PDGF-BB, and TNFα were lower in naringenin treated groups at both 2 weeks (PDGF-BB [0.21% ± 0.03% versus 0.39% ± 0.05% in control group, P < 0.001), TNFα (21.2% ± 0.8% vs. 36.1% ± 1.9% in control group, P < 0.001]) and 4 weeks (PDGF-BB [0.25% ± 0.03% vs. 0.57% ± 0.09% in control group, P < 0.001], TNFα [25.5% ± 1.8% vs. 45.0% ± 2.9% in control group, P < 0.001]). Ki67 LI was lower in naringenin treated groups at 2 weeks (13.9% ± 2.8% vs. 18.7% ± 3.7% in control group, P < 0.05), and at 4 weeks (17.5% ± 2.6% vs. 31.1% ± 4.7% in control group, P < 0.001), indicating a lower level of cellular proliferation.Naringenin reduces NIH following arterial reconstruction. This may be mediated by a decrease in PDGF-BB and TNFα levels and the resulting down-regulation of smooth muscle cells' migration and proliferation.en_US
dc.language.isoEnglishen_US
dc.source.titleAnnals of Plastic Surgeryen_US
dc.relation.isversionofhttp://dx.doi.org/10.1097/SAP.0b013e31819b03cden_US
dc.subjectAnimalsen_US
dc.subjectAntioxidants/pharmacologyen_US
dc.subjectAntioxidants/therapeutic useen_US
dc.subjectDrug Administration Scheduleen_US
dc.subjectFemoral Artery/surgeryen_US
dc.subjectFlavanones/pharmacologyen_US
dc.subjectFlavanones/therapeutic useen_US
dc.subjectHyperplasia/drug therapyen_US
dc.subjectHyperplasia/pathologyen_US
dc.subjectImmunohistochemistryen_US
dc.subjectPostoperative careen_US
dc.subjectRatsen_US
dc.subjectRats, Sprague-Dawleyen_US
dc.subjectReconstructive Surgical Procedures/methodsen_US
dc.subjectTransplantation, Autologousen_US
dc.subjectTunica Intima/drug effectsen_US
dc.subjectTunica Intima/pathologyen_US
dc.subjectVeins/transplantationen_US
dc.titleNaringenin inhibits neointimal hyperplasia following arterial reconstruction with interpositional vein graften_US
dc.typeArticleen_US
dc.departmentUNAM - Institute of Materials Science and Nanotechnology
dc.citation.spage105en_US
dc.citation.epage113en_US
dc.citation.volumeNumber64en_US
dc.citation.issueNumber1en_US
dc.identifier.doi10.1097/SAP.0b013e31819b03cden_US
dc.publisherLippincott Williams & Wilkinsen_US


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