Study Of The Alterations Of Retinal Müller Cell In Short-term Experimental Diabetic Retinopathy

Background and Aim Diabetic Retinopathy (DR) is a serious complication of diabetes and a leading cause of legal blindness in working-age adults. Treatment of diabetic retinopathy is hampered by the lack of understanding of it's pathogenesis. Much of the research effort has been focused on vascular changes. However, little is understood about changes to neurons and neuroglia during the early processes.Müller cell is the main neuroglia in the retina.It can mainly maintain the microenviroment of the retina.The key fuctiong of Müller cell is regulation of extrocellullar glutamate,which is toxic to retina neurons when present in high abundance.Glial fibrillary acidic protein (GFAP) is present in normal Müller cell in several species.Increased GFAP expression reflect glial cell replication.To characterize the morphological and functional changes of Müller cell in short-term experimental diabetic retinopathy by a series kinds of experimentations. To determine whether the Müller cell have played role in diabetic retinopathy and the relationship between Müller cell and retinal microangiopathy.Methods Diabetes was induced in Sprague-Dawley male rats with streptozotocin (STZ, 57mg · kg^-1 body weight). Retinal sample of 4,12 weeks diabetes and controls were prepared for ultrathinsections and subsequently photography by transmissionelectron microscope.Glial fibrillary acidic protein (GFAP) were measured by immunohistochemistry after 4, 12 weeks of STZ-induced diabetes. Using Image System for photo analization. GFAP were measured by Western blot after 4,12 weeks of STZ-induced diabetes.Results Mitochondrial metamorphic in ganglion cell, glia and the neurons of inner nuclear layer occurred in the end of the forth week, and enhanced from then on.GFAP in 4 weeks diabetes weeks diabetes is significantly higher than the controls either in immunohistochemistry and Western blot study .Conclusion The alterations of ultrastructure in retinal neurons and glia approved the abnormalities of morphology in the early phase of diabetes. Increased GFAPshortly after the onset of diabetes indicates the reactivities of glial cells, and the response of neurons to injury.