Astaxanthin (ATX) is a marine carotenoid known for its powerful antioxidant and neuroprotective properties. In this study, we investigated the in vitro and in vivo potential inhibitory effect of ATX on the aldose reductase (AR) activity, a key enzyme in the polyol pathway responsible for the pathogenesis of diabetic complications including diabetic retinopathy (DR). The gerbil Psammomys obesus (P. ob.), an animal model for type 2 diabetes and DR has been used. The erythrocyte and retinal AR activity of P. ob. individuals were, respectively, assessed monthly and at the 7th month during a 7‐month hypercaloric diet (HD) using a NADPH oxidation method. Meanwhile, the body weight and blood glucose of the gerbils were monitored. After 7 months, P. ob. individuals were fed with ATX (4.8 mg/kg of body weight) once a day for 1 week. The results showed that the HD‐fed animals developed significant obesity and hyperglycemia in comparison with controls. Erythrocyte AR activity showed a progressive and significant increase in the HD‐fed group compared with controls. Retinal AR activity was higher in the 7‐month HD‐fed group compared with controls. Erythrocyte AR activity was markedly decreased after ATX‐treatment in vitro and in vivo. These findings suggested that ATX inhibited the erythrocyte AR activity and could be used for DR prevention and/or early treatment.

The purpose of this work was to evaluate a potentially useful animal model, Meriones shawi (M.sh)-developing metabolic X syndrome, diabetes and possessing a visual streak similar to human macula-in the study of diabetic retinopathy and diabetic macular edema (DME). Type 2 diabetes (T2D) was induced by high fat diet administration in M.sh. Body weights, blood glucose levels were monitored throughout the study. Diabetic retinal histopathology was evaluated 3 and 7 months after diabetes induction. Retinal thickness was measured, retinal cell types were labeled by immunohistochemistry and the number of stained elements were quantified. Apoptosis was determined with TUNEL assay. T2D induced progressive changes in retinal histology. A significant decrease of retinal thickness and glial reactivity was observed without an increase in apoptosis rate. Photoreceptor outer segment degeneration was evident, with a significant decrease in the number of all cones and M-cone subtype, but-surprisingly-an increase in S-cones. Damage of the pigment epithelium was also confirmed. A decrease in the number and labeling intensity of parvalbumin- and calretinin-positive amacrine cells and a loss of ganglion cells was detected. Other cell types showed no evident alterations. No DME-like condition was noticed even after 7 months. M.sh could be a useful model to study the evolution of diabetic retinal pathology and to identify the role of hypertension and dyslipidemia in the development of the reported alterations. Longer follow up would be needed to evaluate the potential use of the visual streak in modeling human macular diseases.

No abstract

Our results suggest that the retinal function of Psammomys obesus, especially the cone-mediated function, shares several features with that of human subjects. We believe that Psammomys obesus represents an interesting alternative to study the structure and function of the normal and diseased retina in a human-like rodent model of retinal function.

Astaxanthin is a major marine carotenoid with powerful antioxidant and neuroprotective properties. The in vitro protective effect of astaxanthin in adult retinal cells of the type-2 diabetic model Psammomys obesus in hyperglycemic conditions was investigated. Primary retinal cells were cultured in normal (5 mM) or high concentrations of glucose (25 and 40 mM) for 5 days and treated with 1-20 μM astaxanthin for the last 48 h of culturing. Mitochondrial dehydrogenase activity and cell viability were assessed using MTT test and trypan blue exclusion dye. Retinal cells were characterized by immunohistochemistry. The results showed that mitochondrial function increased significantly (P<0.05) with 5-20 μM astaxanthin in 25-40 mM glucose. At 10 μM astaxanthin, cell viability recovered to 78.51±5.81% and 54.37±9.64% of control in 25 and 40 mM, respectively. Neurons and glial cells expression were enhanced in elevated glucose conditions. These finding suggest that astaxanthin exerted neuroprotection against high glucose induced- retinal damage. Practical Applications: The xanthophyll astaxanthin is found in many marine food sources such as shrimp. The cytoprotective and antioxidant capacity of astaxanthin in retinal disease has been pointed out and presented as a promising therapeutic strategy. The present study shows that astaxanthin can interfere with hyperglycemia-induced retinal cell death and that primary retinal culture of Psammomys obesus may represent an effective system to explore astaxanthin antioxidant mechanisms in diabetic retinopathy