Effect On Retinopathy In Early Period Of Diabetic Rats

Diabetes is a common lifelong disease, and currently there exists a trend that more and more people are having it. Among eye disease caused by diabetes, the diabetic retinopathy has been the most responsible one leading to blindness. For many years, efforts of the diabetic retinopathy diagnosis, treatment, and research have been put on blood vessel lesion. However, little attention has been paid to the change of retinopathy in its early developing stage. The purpose of this study was to examine diabetic retinopathy, in an effort to deepen the understanding and to provide the experimental evidence for improved treatment. In the experiments, pattern electroretinogram (PERG) and flash electroretinogram (FERG) were used to record normal and streptozotocin-induced abnormal PERG-q wave latency and FERG-b wave latency of Diabetic Rats within 8 weeks, respectively. This allows an early examination of the change in the retina function. Also, immunohistochemistry and image processing were applied to investigate 3-nitrotyrosine (NT), the resulting protein product of retinal tissue, thus, providing experimental data for better clinical therapy.The results show that in comparison with normal rats, on the 3rd day of the existence of Diabetic Rat model, the diabetic rats starts to have longer (extended) latency of PERG-q markedly, and since the 1st week, it also has longer latency of PERG-b. In addition, the change occurs earlier in PERG-q than in the FERG-b. In retina of normal rats, no 3-NT was observed; while in retina of diabetic rats, NT were found chiefly in Ganglion cell layer (GCL), and some also exist in inner nuclear layer (INL) and outer nuclear layer (ONL). The image processing results show that in 2, 4 or 8 weeks, there is almost no difference in the number in the retina ofrats. It seems that retina of rats in its early developing stage is able to detect the abnormal visual function via electroretinography before the visual identification of retinopathy. The GCL is the first retinal tissue damaged by diabetes, and then the retina function prior to GCL is subsequently impaired. This indicates that damage of retinal tissue in the diabetes early developing stage is primarily targeted at GCL. Oxidative damage might have significant effect in the course of the diabetic retinopathy development; and the route NO-ONOO-3-NT is involved in pathologic process of the damage of retina.