Abstract
Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness. Available treatments are not completely effective. We analyzed the effect of environmental enrichment on retinal damage induced by experimental diabetes in adult Wistar rats. Diabetes was induced by an intraperitoneal injection of streptozotocin. Three days after vehicle or streptozotocin injection, animals were housed in enriched environment or remained in a standard environment. Retinal function (electroretinogram, and oscillatory potentials), retinal morphology, blood-retinal barrier integrity, synaptophysin, astrocyte and Müller cell glial fibrillary acidic protein, vascular endothelial growth factor, tumor necrosis factor-α, and brain-derived neurotrophic factor levels, as well as lipid peroxidation were assessed in retina from diabetic animals housed in standard or enriched environment. Environmental enrichment preserved scotopic electroretinogram a-wave, b-wave and oscillatory potential amplitude, avoided albumin-Evan's blue leakage, prevented the decrease in retinal synaptophysin and astrocyte glial fibrillary acidic protein levels, the increase in Müller cell glial fibrillary acidic protein, vascular endothelial growth factor and tumor necrosis factor-α levels, as well as oxidative stress induced by diabetes. In addition, enriched environment prevented the decrease in retinal brain-derived neurotrophic factor levels induced by experimental diabetes. When environmental enrichment started 7 weeks after diabetes onset, retinal function was significantly preserved. These results indicate that enriched environment could attenuate the early diabetic damage in the retina from adult rats.
Highlights
Diabetic retinopathy (DR), a leading cause of reduced visual acuity and acquired blindness, is a retinal hyperglycemia-related ischemic disorder characterized by microvascular and neuroglial alterations [1]
The sum of Oscillatory potentials (OPs) amplitudes significantly decreased after 5 weeks of diabetes in animals housed in SE, as compared with vehicle-injected animals, whereas EE housing prevented the effect of diabetes on this parameter (Figure 2C and 2D)
In order to analyze the effect of experimental diabetes and EE on retinal synapses, synaptophysin immunoreactivity was analyzed in retinas from non-diabetic and diabetic animals housed in SE or EE
Summary
Diabetic retinopathy (DR), a leading cause of reduced visual acuity and acquired blindness, is a retinal hyperglycemia-related ischemic disorder characterized by microvascular and neuroglial alterations [1]. The treatments for advanced stages of DR are laser photocoagulation, vitrectomy, and intraocular administration of anti- vascular endothelial growth factor (VEGF) agents, and corticosteroids. These treatments have had considerable success rates, they are not useful for early stages of DR, and do not completely eliminate the risk of blindness (reviewed in [6]). The streptozotocin (STZ)-induced diabetes model in rat shows many of the retinal alterations associated with human DR [7,8]; this model could be a useful tool for developing new therapeutic strategies for DR
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
