The effects of PPAR? agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis model

Basit Öğe Kaydı
dc.contributor.authorGuzeloglu M.
dc.contributor.authorReel B.
dc.contributor.authorAtmaca S.
dc.contributor.authorBagriyanik A.
dc.contributor.authorHazan E.
dc.date.accessioned2019-10-26T21:48:13Z
dc.date.available2019-10-26T21:48:13Z
dc.date.issued2012
dc.departmentEge Üniversitesien_US
dc.description.abstractBackground: Neointimal hyperplasia involving smooth muscle cell (SMC) proliferation, migration and extracellular matrix (ECM) degradation is an important component of atherosclerosis. It develops as a response to vascular injury after balloon angioplasty and vascular graft placement. Matrix metalloproteinases (MMPs) induce SMC proliferation, migration and contribute to intimal hyperplasia by degrading ECM. PPAR? agonists inhibit SMC proliferation, migration and lesion formation. In this study, we aimed to investigate the effects of PPAR? agonist rosiglitazone on neointimal hyperplasia and gelatinase (MMP-2 and MMP-9) expressions in rabbit carotid anastomosis model.Methods: New Zealand white rabbits (n = 13, 2.7-3.2 kg) were divided into placebo and treatment groups. Right carotid artery (CA) was transected and both ends were anastomosed. Treatment group (n = 6) received rosiglitazone (3 mg/kg/day/p.o.) and placebo group (n = 7) received PBS (phosphate buffered saline, 2.5 ml/kg/day/p.o.) for 4 weeks postoperatively. After the sacrification, right and left CAs were isolated. Morphometric analyses and immunohistochemical examinations for gelatinases were performed.Results: Intimal area (0.055 ± 0.005 control vs 0.291 ± 0.020 µm 2 anastomosed, p < 0,05) and index (0.117 ± 0.002 control vs 0.574 ± 0.013 anastomosed, p < 0,01) significantly increased in anastomosed arteries compared to control arteries from placebo group. However, in rosiglitazone-treated group, intimal area (0.291 ± 0.020 PBS vs 0.143 ± 0.027 rosiglitazone, p < 0,05) and index (0.574 ± 0.013 PBS vs 0.263 ± 0.0078 rosiglitazone, p < 0,01) significantly decreased. Furthermore, gelatinase immunopositivity was found to have significantly increased in anastomosed arteries from placebo group and decreased with rosiglitazone treatment.Conclusions: These results suggest that rosiglitazone may prevent neointimal hyperplasia, which is the most important factor involved in late graft failure, by inhibiting gelatinase enzyme expression. © 2012 Guzeloglu et al.; licensee BioMed Central Ltd.en_US
dc.identifier.doi10.1186/1749-8090-7-57en_US
dc.identifier.issn1749-8090
dc.identifier.issue1en_US
dc.identifier.pmid22716287en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1186/1749-8090-7-57
dc.identifier.urihttps://hdl.handle.net/11454/18647
dc.identifier.volume7en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.relation.ispartofJournal of Cardiothoracic Surgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectMatrix metalloproteinases (MMPs)en_US
dc.subjectNeointimaen_US
dc.subjectRabbiten_US
dc.subjectRosiglitazoneen_US
dc.titleThe effects of PPAR? agonist rosiglitazone on neointimal hyperplasia in rabbit carotid anastomosis modelen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

Scopus İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu