Effect of Tianeptine on Oxidative Renal Damage Induced by Ischemia Reperfusion in Rats

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Özet

Renal ischemia-reperfusion (I/R) damage can develop following major surgical conditions such as shock, trauma, and renal transplantation and causes acute renal failure. Kidney I/R damage is known to be a pathological process that begins with the touch free of oxygen and continues with the production of free oxygen radicals. We will investigate the effect of renal I/R injury on tianeptine, an atypical antidepressant drug with antioxidant properties. There was no information on the effect of tianeptine on I/R-induced kidney damage in the literature. The aim of the present study was to investigate the effect of tianeptine on oxidative kidney damage induced by I/R in rats. Albino wistar male rats were divided into groups as renal I/R (RIR) group, 25 mg/kg of thianeptine+renal I/R (TIR-25) group and sham operation (SG) group. The I/R procedure (one hour ischemia, three hours reperfusion) was performed with 25 mg/kg intraperitoneal thiopental sodium anesthesia. Oxidative damage was assessed by malondialdehyde (MDA) and total glutathione (TGSH) measurements in kidney tissue. Biochemical test results showed that the I/R process increased the amount of MDA in the kidney tissue and decreased the tGSH. Tianeptine significantly prevented the increase of MDA and decrease of tGSH in kidney tissue after I/R. Our experimental results suggest that tianeptine may be useful in preventing I/Rinduced oxidative renal injury.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/22504Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.18185/erzifbed.422543Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorBilgin, Aslı Özbek
dc.contributor.authorSüleyman, Bahadır
dc.contributor.authorMammadov, Renad
dc.date.accessioned2026-10-20T11:09:41.384206828Z
dc.date.available2026-10-20T11:09:41.384206828Z
dc.date.issued2018
dc.description.abstractRenal ischemia-reperfusion (I/R) damage can develop following major surgical conditions such as shock, trauma, and renal transplantation and causes acute renal failure. Kidney I/R damage is known to be a pathological process that begins with the touch free of oxygen and continues with the production of free oxygen radicals. We will investigate the effect of renal I/R injury on tianeptine, an atypical antidepressant drug with antioxidant properties. There was no information on the effect of tianeptine on I/R-induced kidney damage in the literature. The aim of the present study was to investigate the effect of tianeptine on oxidative kidney damage induced by I/R in rats. Albino wistar male rats were divided into groups as renal I/R (RIR) group, 25 mg/kg of thianeptine+renal I/R (TIR-25) group and sham operation (SG) group. The I/R procedure (one hour ischemia, three hours reperfusion) was performed with 25 mg/kg intraperitoneal thiopental sodium anesthesia. Oxidative damage was assessed by malondialdehyde (MDA) and total glutathione (TGSH) measurements in kidney tissue. Biochemical test results showed that the I/R process increased the amount of MDA in the kidney tissue and decreased the tGSH. Tianeptine significantly prevented the increase of MDA and decrease of tGSH in kidney tissue after I/R. Our experimental results suggest that tianeptine may be useful in preventing I/Rinduced oxidative renal injury.
dc.identifier.doi10.18185/erzifbed.422543
dc.identifier.eissn2149-4584
dc.identifier.endpage305
dc.identifier.issn1307-9085
dc.identifier.issue2
dc.identifier.startpage300
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/22504
dc.identifier.volume11
dc.language.isotr
dc.relation.ispartofErzincan Üniversitesi Fen Bilimleri Enstitüsü Dergisi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectTıbbi Araştırmalar Deneysel
dc.subjectGenel ve Dahili Tıp
dc.subjectYoğun Bakım, Tıp
dc.titleEffect of Tianeptine on Oxidative Renal Damage Induced by Ischemia Reperfusion in Rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.trdizin1
rdl.source.indexTRDIZIN