Carvacrol reduces the severity of intestinal mucosal damage caused by intestinal ischemia - Reperfusion in rats

Basit Öğe Kaydı
dc.authorid0000-0002-8212-7149en_US
dc.authorid0000-0001-6768-1275en_US
dc.authorid0000-0002-7006-3125en_US
dc.contributor.authorÖztürk, Hülya
dc.contributor.authorÇetinkaya, Ayhan
dc.contributor.authorDüzcü, Selma Erdoğan
dc.contributor.authorYis, Özgür Mehmet
dc.contributor.authorÖztürk, Hayrettin
dc.date.accessioned2021-06-23T19:50:55Z
dc.date.available2021-06-23T19:50:55Z
dc.date.issued2019
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractIntestinal ischemia-reperfusion (I/R) is a pathophysiological process that is common in many clinical conditions such as shock, sepsis, mesenteric thrombosis, necrotizing enterocolitis, and bowel transplantation. Our aim in this study was to investigate the potential protective effects of carvacrol on the intestinal I/R injury in a rat model. The 30 rats were randomly divided into three groups (n = 10): The sham-control (group 1) underwent only the separation of the superior mesenteric artery but not the occlusion. In the FR-untreated (group 2) and I/R-carvacrol-treated groups (group 3), the superior mesenteric artery was clamped for 45 min, followed by 60 min of reperfusion. 2 hours before ischemia, the group 3 of rats received an intraperitoneal injection of carvacrol at a dose of 75 mg/kg bw. At the end of the experiment, intestinal tissue samples were taken for oxidative stress assessment including superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), total antioxidant status (TAS) and total oxidant status (TOS). In addition, the intestine sections were stained with haematoxylin-eosin to evaluate morphological changes and immunohistochemical staining was performed for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) assessment. The intestinal mucosa was significantly damaged in the group 2, which was markedly attenuated after carvacrol treatment. The tissue MDA, MPO and TOS content increased significantly in the group 2, but they were reduced by carvacrol treatment. In addition, SOD and TAS activity increased markedly in group 3 as compared to group 2. Immunohistochemical staining showed that iNOS increased and eNOS decreased in group 2, which was improved in reverse direction after carvacrol treatment. Carvacrol may be a potential therapeutic agent for the treatment of intestinal I/R injury.en_US
dc.identifier.doi10.31925/farmacia.2019.5.21
dc.identifier.endpage898en_US
dc.identifier.issn0014-8237
dc.identifier.issn2065-0019
dc.identifier.issue5en_US
dc.identifier.scopus2-s2.0-85073510673en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage892en_US
dc.identifier.urihttps://doi.org/10.31925/farmacia.2019.5.21
dc.identifier.urihttps://hdl.handle.net/20.500.12491/9889
dc.identifier.volume67en_US
dc.identifier.wosWOS:000489127500021en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorÖztürk, Hülya
dc.institutionauthorÇetinkaya, Ayhan
dc.institutionauthorDüzcü, Selma Erdoğan
dc.institutionauthorYis, Özgür Mehmet
dc.institutionauthorÖztürk, Hayrettin
dc.language.isoenen_US
dc.publisherSoc Stiinte Farmaceutice Romaniaen_US
dc.relation.ispartofFarmaciaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCarvacrolen_US
dc.subjectIschemia-Reperfusion Injuryen_US
dc.subjectOxidative Stressen_US
dc.subjectIntestineen_US
dc.subjectRaten_US
dc.titleCarvacrol reduces the severity of intestinal mucosal damage caused by intestinal ischemia - Reperfusion in ratsen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim
İsim:
hulya-ozturk.pdf
Boyut:
232.55 KB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin/Full Text
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
Cerrahi Tıp Bilimleri Bölümü Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu
Temel Tıp Bilimleri Bölümü Koleksiyonu