Oral carnosine supplementation prevents vascular damage in experimental diabetic retinopathy

BACKGROUNDS/AIMS: Pericyte loss, vasoregression and neuroglial activation are characteristic changes in incipient diabetic retinopathy. In this study, the effect of the antioxidant and antiglycating dipeptide carnosine was studied on the development of experimental diabetic retinopathy. - MATERIALS/...

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Hauptverfasser: Pfister, Frederick (VerfasserIn) , Riedl, Eva (VerfasserIn) , Wang, Qian (VerfasserIn) , vom Hagen, Franziska (VerfasserIn) , Deinzer, Martina Ulrike (VerfasserIn) , Harmsen, Martin Conrad (VerfasserIn) , Molema, Grietje (VerfasserIn) , Yard, Benito A. (VerfasserIn) , Feng, Yuxi (VerfasserIn) , Hammes, Hans-Peter (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: August 16, 2011
In: Cellular physiology and biochemistry
Year: 2011, Jahrgang: 28, Heft: 1, Pages: 125-136
ISSN:1421-9778
DOI:10.1159/000331721
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1159/000331721
Volltext
Verfasserangaben:Frederick Pfister, Eva Riedl, Qian Wang, Franziska vom Hagen, Martina Deinzer, Martin Conrad Harmsen, Grietje Molema, Benito Yard, Yuxi Feng and Hans-Peter Hammes

MARC

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520 |a BACKGROUNDS/AIMS: Pericyte loss, vasoregression and neuroglial activation are characteristic changes in incipient diabetic retinopathy. In this study, the effect of the antioxidant and antiglycating dipeptide carnosine was studied on the development of experimental diabetic retinopathy. - MATERIALS/METHODS: STZ-induced diabetic Wistar rats were orally treated with carnosine (1g/kg body weight/day). Retinal vascular damage was assessed by quantitative morphometry. Retinal protein extracts were analyzed for markers of oxidative stress, AGE-formation, activation of the hexosamine pathway and changes in the expression of Ang-2, VEGF and heat shock proteins Hsp27 and HO-1. Glial cell activation was analyzed using Western blot analysis and immunofluorescence of GFAP expression and retinal neuronal damage was histologically examined. - RESULTS: Oral carnosine treatment prevented retinal vascular damage after 6 months of experimental hyperglycemia. The protection was not caused by ROS- or AGE-inhibition, but associated with a significant induction of Hsp27 in activated glial cells and normalization of increased Ang-2 levels in diabetic retinas. A significant reduction of photoreceptors in retinas of carnosine treated animals was noted. - CONCLUSION: Oral carnosine treatment protects retinal capillary cells in experimental diabetic retinopathy, independent of its biochemical function. The vasoprotective effect of carnosine might be mediated by the induction of protective Hsp27 in activated glial cells and normalization of hyperglycemia-induced Ang-2. 
650 4 |a Administration, Oral 
650 4 |a Angiopoietin-2 
650 4 |a Animals 
650 4 |a Antioxidants 
650 4 |a Carnosine 
650 4 |a Diabetes Mellitus, Experimental 
650 4 |a Disease Models, Animal 
650 4 |a Glycation End Products, Advanced 
650 4 |a Heme Oxygenase-1 
650 4 |a HSP27 Heat-Shock Proteins 
650 4 |a Male 
650 4 |a Neuroglia 
650 4 |a Oxidative Stress 
650 4 |a Pericytes 
650 4 |a Photoreceptor Cells, Vertebrate 
650 4 |a Rats 
650 4 |a Rats, Wistar 
650 4 |a Reactive Oxygen Species 
650 4 |a Retinal Ganglion Cells 
650 4 |a Retinal Vessels 
650 4 |a Streptozocin 
650 4 |a Vascular Endothelial Growth Factor A 
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