title: Pleiotropic and Renoprotective Effects of Erythropoietin Beta on Experimental Diabetic Nephropathy Model.
abstract: BACKGROUND
  This study aimed at investigating the possible protective effect of erythropoietin beta on experimental diabetic nephropathy (DN) model in rats.
  
  
  METHODS
  Sprague Dawley rats (n = 32) were allocated into 4 equal groups of 8 each, the control (Group C), diabetes (Group D), erythropoietin beta (Group E), and erythropoietin beta treated DN (Group E + D) groups. Streptozocin (65 mg/kg) was used to induce diabetes in 10-week old rats. Erythropoietin beta was given intraperitoneally at a dose of 500 IU/kg/3 days of a week for 12 weeks. Renal function parameters, intrarenal levels and activities of oxidative stress biomarkers, serum inflammatory parameters and kidney histology were determined.
  
  
  RESULTS
  Group E + D had lower mean albumin-to-creatinine ratio (p < 0.001) as well as higher creatinine clearance (p = 0.035) than the diabetic rats (Group D). Intrarenal malondialdehyde levels were significantly lower (p = 0.004); glutathione (GSH) levels (p = 0.003), GSH peroxidase (p = 0.004) and superoxide dismutase (p < 0.005) activities of renal tissue were significantly higher in Group E + D than in Group D. The mean serum levels of interleukin-4 (p < 0.005), interleukin 1 beta (p = 0.012), interferon gamma (p = 0.018) and tumor necrosis factor alpha (p < 0.005) were significantly lower; serum levels of monocyte chemoattractant protein 1 (p = 0.018) was significantly higher in Group E + D when compared to Group D. The mean scores of tubulointerstitial inflammation (p = 0.004), tubular injury (p = 0.013) and interstitial fibrosis (p = 0.003) were also lower in Group E + D when compared to Group D.
  
  
  CONCLUSIONS
  Our data seem to suggest a potential role of erythropoietin beta for reducing the progression of DN in an experimental rat model. This protective effect is, in part, attributable to the suppression of the inflammatory response and oxidative damage.
authors.affiliation: Department of Physiology, Medipol University, Medical Faculty, Istanbul, Turkey.
authors.forename: Zehra
authors.initials: Z
authors.lastname: Eren
authors.forename: Mehmet Yalçın
authors.initials: MY
authors.lastname: Günal
authors.forename: Elif
authors.initials: E
authors.lastname: Arı
authors.forename: Jale
authors.initials: J
authors.lastname: Çoban
authors.forename: Fulya
authors.initials: F
authors.lastname: Çakalağaoğlu
authors.forename: Burak
authors.initials: B
authors.lastname: Çağlayan
authors.forename: Mustafa Çağlar
authors.initials: MÇ
authors.lastname: Beker
authors.forename: Tuba
authors.initials: T
authors.lastname: Akdeniz
authors.forename: Gülderen
authors.initials: G
authors.lastname: Yanıkkaya
authors.forename: Ertuğrul
authors.initials: E
authors.lastname: Kılıç
authors.forename: Gülçin
authors.initials: G
authors.lastname: Kantarcı
mesh_terms: D000818:Animals; D016207:Cytokines / Q000097:blood; D003928:Diabetic Nephropathies / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D004195:Disease Models, Animal; D004921:Erythropoietin / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D004921:Erythropoietin; D013482:Superoxide Dismutase; D005978:Glutathione