The effects of PPAR-? agonist pioglitazone on renal ischemia/reperfusion injury in rats

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dc.contributor.authorReel B.
dc.contributor.authorGuzeloglu M.
dc.contributor.authorBagriyanik A.
dc.contributor.authorAtmaca S.
dc.contributor.authorAykut K.
dc.contributor.authorAlbayrak G.
dc.contributor.authorHazan E.
dc.date.accessioned2019-10-27T08:23:40Z
dc.date.available2019-10-27T08:23:40Z
dc.date.issued2013
dc.departmentEge Üniversitesien_US
dc.description.abstractBackground: Acute renal failure due to renal ischemia/reperfusion (IR) injury is a significant clinical problem in cardiovascular surgery. Reactive oxygen species and inflammation play essential roles in the pathophysiology of IR injury. Matrix metalloproteinases (MMPs) are enzymes that play important roles in inflammation and mediate extracellular matrix degradation. It is known that peroxisome proliferator-activated receptor-? agonists have antiinflammatory and antioxidant effects. In the present study, we aimed to investigate the effects of pioglitazone, a synthetic peroxisome proliferator-activated receptor-? agonist, on MMPs and oxidative stress in a renal IR injury model in rats. Materials and methods: Male Wistar albino rats were divided into three groups: control (n = 7), placebo (n = 7; saline/p.o.), and pioglitazone (n = 7; 5 mg/kg/day/p.o.). In the control group, a right nephrectomy was conducted without left renal IR injury. In the placebo and pioglitazone groups, pretreatments were started 3 d before operation. In both groups, left renal pedicles were clamped for 60 min and then reperfused for 60 min. Paraffinized renal sections were evaluated histopathologically. Furthermore, expressions of MMP-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-2, superoxide dismutase 1 (SOD1), and p47-phox/p67-phox subunits of NADPH oxidase were determined by immunostaining and scoring. Results: In the placebo group, renal IR injury induced diffuse tubular necrosis and intense acute inflammation, but pioglitazone inhibited these effects. MMP-2, MMP-9, and TIMP-2 expression increased in the placebo group. However, while MMP-2 and -9 expression decreased, TIMP-2 expression did not change in the pioglitazone group. p47-phox/p67-phox expression increased in the placebo group, but SOD1 expression did not change. Pioglitazone diminished p47-phox/p67-phox expression, whereas it enhanced SOD1 expression. Conclusion: Our results suggest that pioglitazone might be helpful to reduce renal IR injury because of its antiinflammatory and antioxidant effects.en_US
dc.identifier.doi10.1016/j.jss.2012.08.020en_US
dc.identifier.endpage184en_US
dc.identifier.issn0022-4804
dc.identifier.issue1en_US
dc.identifier.pmid22981741en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage176en_US
dc.identifier.urihttps://doi.org/10.1016/j.jss.2012.08.020
dc.identifier.urihttps://hdl.handle.net/11454/26463
dc.identifier.volume182en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.relation.ispartofJournal of Surgical Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectInflammationen_US
dc.subjectMMPen_US
dc.subjectOxidative stressen_US
dc.subjectPPAR-? agonisten_US
dc.subjectRenal ischemia/reperfusionen_US
dc.titleThe effects of PPAR-? agonist pioglitazone on renal ischemia/reperfusion injury in ratsen_US
dc.typeArticleen_US

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