Ellagic Acid Inhibits TGF?1/Smad-Induced Renal Fibrosis in Diabetic Kidney Injury

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dc.contributor.authorYıldız, Halime Tozak
dc.contributor.authorSarıbaş, Gülistan Sanem
dc.contributor.authorNone, Ozkan
dc.date.accessioned2023-04-10T20:21:03Z
dc.date.available2023-04-10T20:21:03Z
dc.date.issued2022
dc.departmentRektörlük, Rektörlüğe Bağlı Birimler, Düzce Üniversitesi Dergilerien_US
dc.description.abstractAim: Free radical formation increases due to hyperglycemia occurring in the pathogenesis of diabetes mellitus (DM), and as a result, oxidative stress occurs. Hyperglycemia-mediated oxidative stress plays an important role in the pathogenesis of diabetic nephropathy. The antihyperglycemic, antioxidative, anti-apoptotic, and anti-inflammatory effects of ellagic acid (EA) have been demonstrated by many studies. In this study, it was aimed to demonstrate the antifibrotic effect of EA on TGF?1/Smad signaling in rats with streptozotocin induced diabetic nephropathy. Material and Methods: A total of 24 male Sprague Dawley rats, weighing 200-250 g, were used in this study. The animals were divided into four groups as control, EA, DM, and DM+EA. The kidney tissues were used for histological and immunohistochemical procedures. While the collagen density in kidney tissues was revealed by Masson's trichrome staining, the expression levels of fibrotic markers TGF?1, p-Smad3, and ?SMA were determined by the immunocytochemical method. Results: It was shown that the collagen density in the renal tissue of the DM group increased significantly in the intertubular area, while the collagen density in the EA-treated DM group was statistically significantly decreased. When TGF?1, p-Smad3, and ?SMA immunopositivity in kidney tissue sections of all groups were evaluated, the highest staining intensity was in the DM group, while the intensity of staining was close to the control group in the treatment group. It was observed that ?SMA, TGF?1, and p-Smad3 protein expression were down-regulated with EA treatment. Conclusion: EA reduced fibrosis in diabetic nephropathy by returning profibrotic parameters to normal levels.en_US
dc.identifier.doi10.18678/dtfd.1198021
dc.identifier.endpage327en_US
dc.identifier.issn1307-671X
dc.identifier.issue3en_US
dc.identifier.startpage321en_US
dc.identifier.trdizinid1146384en_US
dc.identifier.urihttp://doi.org/10.18678/dtfd.1198021
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/1146384
dc.identifier.urihttps://hdl.handle.net/20.500.12684/11536
dc.identifier.volume24en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofDüzce Tıp Fakültesi Dergisien_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDiabetes mellitusen_US
dc.subjectellagic aciden_US
dc.subjectfibrosisen_US
dc.subjectkidneyen_US
dc.subjectTGF?/Smad Diabetes mellitusen_US
dc.subjectelajik asiten_US
dc.subjectfibrozisen_US
dc.subjectböbreken_US
dc.subjectTGF?/smaden_US
dc.titleEllagic Acid Inhibits TGF?1/Smad-Induced Renal Fibrosis in Diabetic Kidney Injuryen_US
dc.typeArticleen_US

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