Trimetazidine increases cell survival and inhibits the activation of inflammatory response in sodium taurocholate-induced acute pancreatitis

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dc.authorid0000-0001-9149-9510en_US
dc.authorid0000-0002-3535-6977
dc.authorid0000-0002-3487-1264
dc.authorid0000-0001-5912-9392
dc.authorid0000-0002-8317-7092
dc.contributor.authorIşık, Sevil
dc.contributor.authorŞengül, Neriman
dc.contributor.authorTöre, Fatma
dc.contributor.authorAydın, Cemalettin
dc.contributor.authorAslan, Açelya
dc.contributor.authorFırat, Tülin
dc.contributor.authorKükner, Aysel
dc.contributor.authorBayram, Recep
dc.date.accessioned2021-06-23T19:45:14Z
dc.date.available2021-06-23T19:45:14Z
dc.date.issued2017
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractObjective: To evaluate the therapeutic effects of trimetazidine (TMZ) in an experimental acute pancreatitis (AP) model induced with sodium taurocholate (STC). Summary of Background Data: At present, AP is considered a disease with no specific treatment. Preventing mitochondrial dysfunction in acinar cells may be an option for specific treatment of AP. TMZ is an anti-ischemic drug with anti-inflammatory, antioxidant, and mitochondrial modulatory effects. Methods: Rats were divided into 4 groups. AP was induced in the AP (n = 7) and AP + TMZ (n = 7) groups by an injection of 4% sodium taurocholate to the pancreatic duct. The sham (n = 6) and drug (n = 6) groups were designated as control groups. The AP + TMZ and drug groups were administered TMZ. Samples were taken at 72 hours, and histopathologic changes as well as biochemical parameters were analyzed. Results: Serum amylase, tissue myeloperoxidase activity, malondialdehyde levels, serum cytokine levels, and mast cell degranulation rates were elevated after induction of AP, whereas tissue antioxidant enzyme activities and cell viability rates [determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay] decreased. These parameters were found to be different in the AP group compared with those in all other groups (P < 0.05). A significant improvement of all parameters was achieved with the TMZ treatment of AP. Histologically, significant differences were found between the AP and AP + TMZ groups in terms of leukocyte infiltration, necrosis, and apoptotic cell counts. Conclusions: In this study, we demonstrated that TMZ treatment protected the mitochondrial function and prevented the activation of the inflammatory cascade in the sodium taurocholate-induced AP model.en_US
dc.identifier.doi10.9738/INTSURG-D-17-00122.1
dc.identifier.endpage551en_US
dc.identifier.issn0020-8868
dc.identifier.issue11-12en_US
dc.identifier.scopus2-s2.0-85063218261en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage542en_US
dc.identifier.urihttps://doi.org/10.9738/INTSURG-D-17-00122.1
dc.identifier.urihttps://hdl.handle.net/20.500.12491/9121
dc.identifier.volume102en_US
dc.identifier.wosWOS:000460124300010en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorŞengül, Neriman
dc.institutionauthorFırat, Tülin
dc.institutionauthorKükner, Aysel
dc.institutionauthorBayram, Recep
dc.language.isoenen_US
dc.publisherInt College Of Surgeonsen_US
dc.relation.ispartofInternational Surgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAcute Pancreatitisen_US
dc.subjectMitochondriaen_US
dc.subjectTrimetazidineen_US
dc.subjectMast Cellen_US
dc.subjectOxidative Stressen_US
dc.subjectExperimentalen_US
dc.titleTrimetazidine increases cell survival and inhibits the activation of inflammatory response in sodium taurocholate-induced acute pancreatitisen_US
dc.typeArticleen_US

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