The aim of this study is to evaluate the effect of intravitreal anti VEGF single injection on retinal architecture and edema in diabetic mice. Methods: The study included 39 non-obese diabetic (NOD) mice, aged 4-8 months, all examined for glucose levels in the blood. Ten underwent in vivo fluorescein angiography (FA) to demonstrate retinal blood flow and leakage; 8 NOD mice, 4 diabetic and 4 non-diabetics, were perfused with fluorescent gelatin to establish co-localization of vascular stains with vessel lumens. The remaining 21 were divided to 3 subgroups. Seven mice were included in each group which was administered either bevacizumab (Avastin), or saline 0.9% intravitreal injection to the right eye and the left eye served as an internal control. The last group was not treated. All mice were analyzed histologically, stained for Hematoxylin Eosin and Periodic acid–Schiff (PAS) and by immunohistochemistry staining for vascular and neuronal markers (Vimentin, GFAP and NG-2). The 7 control mice (untreated group) were also analyzed molecularly. Molecular tests were examined for the following gene levels of expression: Vimentin, GFAP, VEGF and VEGF/R-1,2, RAGE, EPO.
In vivo FA did not reveal neovascularization. However, perfusion showed tufts suspected for neovascularization, as well as microaneurysms and tortured blood vessels in the diabetic NOD mice only. Retinal thickness was measured in the 3 groups, as follows: without treatment 289μm + 20, Saline 308μm + 27 in both eyes and Avastin 219μm + 51 in the right vs. 270μm + 28 in the left eye. Molecular analysis showed an increase only in RAGE (2.7105 vs. 1), while the others remained at baseline levels and VEGF was reduced to 0.5, in the diabetic Vs non diabetic NOD mice.
Different thickness of retina was found in treated vs. untreated mice. Although VEGF levels did not increase in the diabetic mice, the antiVEGF treatment reduced retinal edema and improved diabetic retinopathy in NOD mice