April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Enriched environment protects the retina from diabetic damage in adult rats
Author Affiliations & Notes
  • Damian Dorfman
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Marcos L Aranda
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Maria F Gonzalez Fleitas
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Monica Chianelli
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Diego Carlos Fernandez
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Ruth Estela Rosenstein
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships Damian Dorfman, None; Marcos Aranda, None; Maria Gonzalez Fleitas, None; Monica Chianelli, None; Diego Fernandez, None; Ruth Rosenstein, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4915. doi:
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    • Get Citation

      Damian Dorfman, Marcos L Aranda, Maria F Gonzalez Fleitas, Monica Chianelli, Diego Carlos Fernandez, Ruth Estela Rosenstein; Enriched environment protects the retina from diabetic damage in adult rats. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4915.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Diabetic retinopathy (DR) is a leading cause of acquired blindness. Available treatments are not very effective. Enriched environment (EE) allows freedom to move and exercise voluntarily in larger cage, with accessibility to complex stimuli as well as social interaction. We investigated the effect of EE housing on retinal damage induced by experimental diabetes.

Methods: Diabetes was induced by an intraperitoneal injection of streptozotocin (STZ). EE consisted of big cages housing 6 animals, and containing several food hoppers, wheels and different objects repositioned once/day and fully substituted once/week. DR was evaluated in terms of: i) retinal function (electroretinogram (ERG) and oscillatory potentials (OPs)), ii) integrity of blood- retinal barrier (by albumin-Evan’s Blue complex leakage and astrocyte glial fibrillary acidic protein (GFAP) immunohistochemistry), iii) vascular endothelial growth factor (VEGF) levels (by Western blot and immunohistochemistry), and iv) retinal lipid peroxidation (thiobarbituric acid reactive substances, TBARS).

Results: EE significantly preserved ERG a- and b-wave and OPs, avoided albumin-Evan’s blue leakage, and prevented the decrease in astrocyte GFAP levels in diabetic rats. EE prevented the increase in VEGF and TBARS levels induced by experimental diabetes. When EE housing started 7 weeks after diabetes onset, retinal function was significantly preserved.

Conclusions: These results indicate that EE housing could become a novel and harmless therapeutic strategy in DR treatment.

Keywords: 499 diabetic retinopathy • 615 neuroprotection • 748 vascular endothelial growth factor  
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