Does sucralfate prevent apoptosis occurring in the ischemia/reperfusion-induced intestinal injury?

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dc.contributor.authorŞencan A.
dc.contributor.authorYilmaz Ö.
dc.contributor.authorÖzer E.
dc.contributor.authorGünşar C.
dc.contributor.authorGenç K.
dc.contributor.authorUlukuş Ç.
dc.contributor.authorTaneli C.
dc.contributor.authorMir E.
dc.date.accessioned2024-07-22T08:24:44Z
dc.date.available2024-07-22T08:24:44Z
dc.date.issued2003
dc.description.abstractBackground/Purpose: We have shown in a previous study that sucralfate is beneficial in the prophylaxis and treatment of hypoxia/reoxygenation-induced intestinal injury. The aim of this study is to investigate whether sucralfate has any effect on the prevention of apoptosis in the ischemia/reperfusion (I/R)-induced intestinal injury. Methods: Rats were randomized into three groups. Group 1 and 2 were subjected to I/R. Group 1 (treatment group) received sucralfate while group 2 (treatment control group) did not. Group 3 served as a normal control group (sham group). The terminal ileum was harvested for histopathologic investigation by light microscopy. The presence of apoptotic enterocytes (DNA fragmentation in cell nuclei) was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end-labeling (TUNEL) reaction. Results: In treatment control group, 3 of 7 rats had severe inflammation. None of the sucralfate-treated rats showed severe inflammation, 6 of them only showed mild inflammatory changes (p < 0.05). The apoptotic percentage was found to be 37.1 ± 9.4 in the sucralfate-treated group (group 1), whereas it was 45.4 ± 3.9 in the untreated group (group 2) (p < 0.05). The sham group had a completely normal intestinal architecture. Conclusions: The present study shows that 1) the experimental model of I/R-induced intestinal injury induces enterocyte apoptosis; 2) sucralfate decreases enterocyte apoptosis in the experimental model of I/R-induced intestinal injury which may play a key role in the pathophysiological events leading to failure of the intrinsic gut barrier defense mechanisms.
dc.identifier.DOI-ID10.1055/s-2003-42235
dc.identifier.issn09397248
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/20089
dc.language.isoEnglish
dc.subjectAnimals
dc.subjectAnti-Ulcer Agents
dc.subjectApoptosis
dc.subjectEnterocytes
dc.subjectIntestinal Diseases
dc.subjectIntestines
dc.subjectModels, Animal
dc.subjectRandom Allocation
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReperfusion Injury
dc.subjectSucralfate
dc.subjectcell DNA
dc.subjectDNA fragment
dc.subjectsucralfate
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectapoptosis
dc.subjectarticle
dc.subjectcell nucleus
dc.subjectcontrolled study
dc.subjectdrug effect
dc.subjecthistopathology
dc.subjectileum
dc.subjectinflammation
dc.subjectintestine cell
dc.subjectintestine injury
dc.subjectintestine ischemia
dc.subjectmicroscopy
dc.subjectnecrotizing enterocolitis
dc.subjectnick end labeling
dc.subjectnonhuman
dc.subjectpathophysiology
dc.subjectprophylaxis
dc.subjectrat
dc.subjectreperfusion injury
dc.titleDoes sucralfate prevent apoptosis occurring in the ischemia/reperfusion-induced intestinal injury?
dc.typeArticle

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