Effects of Carvacrol in an Experimentally Induced Esophageal Burn Model: Expression of VEGF and Caspase-3 Proteins

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dc.contributor.authorZeytun, Hikmet
dc.contributor.authorOzkorkmaz, Ebru Gokalp
dc.date.accessioned2024-04-24T16:24:40Z
dc.date.available2024-04-24T16:24:40Z
dc.date.issued2021
dc.departmentDicle Üniversitesien_US
dc.description.abstractIntroduction: We investigated the therapeutic effects of carvacrol in an experimental esophageal burn rat model with immunohistochemical techniques. Materials and Methods: Three groups were included in this study, composed of eight Wistar albino rats each. The control group was given 1 mL 0.9% (wt/vol) NaCl; esophageal burns were induced in groups 2 and 3 by administration of 1 mL 40% NaOH in the distal 2 cm of the esophagus. The treatment group was administered 75 mg/kg carvacrol in 2 mL 0.9% NaCl for 10 days. After a routine histological examination of the tissues, sections were stained with vascular endothelial growth factor (VEGF) and caspase-3 for immunohistochemical analysis and were examined under a light microscope. Results: In the control group, there were regular cells in the cornified epithelial tissue and cylindrical cells in the basal layer, which faced toward the apical surface in the mitotic phase. The burn group displayed wide degeneration, necrosis, and abundant apoptotic cells in the epithelial tissue as well as intense inflammatory cell infiltration. In the treatment group, there was an increase in mitotic activity in the basal cells of the epithelial layer and degenerative changes, but a preserved epithelial layer and significant cornified structures. The treatment group showed positive caspase-3 expression in some apoptotic cells within the epithelial layer and in connective tissue, and there were only a small number of degenerated cells in the muscle layer. Additionally, in the treatment group, VEGF expression was evident in small numbers of inflammatory cells in the papillary region of the epithelium, and in dilated vascular endothelial cells. Conclusions: Carvacrol may contribute to a reduction in fibrosis by decreasing inflammation and preventing cell apoptosis.en_US
dc.identifier.doi10.1080/08941939.2019.1637484
dc.identifier.endpage416en_US
dc.identifier.issn0894-1939
dc.identifier.issn1521-0553
dc.identifier.issue4en_US
dc.identifier.pmid31288583
dc.identifier.scopus2-s2.0-85068697872
dc.identifier.scopusqualityQ1
dc.identifier.startpage408en_US
dc.identifier.urihttps://doi.org/10.1080/08941939.2019.1637484
dc.identifier.urihttps://hdl.handle.net/11468/16812
dc.identifier.volume34en_US
dc.identifier.wosWOS:000475049000001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofJournal of Investigative Surgery
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCarvacrolen_US
dc.subjectCaspase-3en_US
dc.subjectEsophageal Burnen_US
dc.subjectImmunohistochemistryen_US
dc.subjectRaten_US
dc.subjectVegfen_US
dc.titleEffects of Carvacrol in an Experimentally Induced Esophageal Burn Model: Expression of VEGF and Caspase-3 Proteinsen_US
dc.titleEffects of Carvacrol in an Experimentally Induced Esophageal Burn Model: Expression of VEGF and Caspase-3 Proteins
dc.typeArticleen_US

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