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首页> 外文期刊>CNS neuroscience & therapeutics. >Upregulation of Glutamate–Aspartate Transporter by Glial Cell Line–Derived Neurotrophic Factor Ameliorates Cell Apoptosis in Neural Retina in Streptozotocin‐Induced Diabetic Rats
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Upregulation of Glutamate–Aspartate Transporter by Glial Cell Line–Derived Neurotrophic Factor Ameliorates Cell Apoptosis in Neural Retina in Streptozotocin‐Induced Diabetic Rats

机译：胶质细胞源性神经营养因子对谷氨酸-天冬氨酸转运蛋白的上调改善了链脲佐菌素诱导的糖尿病大鼠神经视网膜中的细胞凋亡。

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Summary Aims Dysfunction of glutamate uptake, largely mediated by the glutamate–aspartate transporter ( GLAST ), may lead to retinal cell apoptosis in diabetic retinopathy. The aim of this study is to examine how cell apoptosis and the expression level of GLAST in neural retina of a diabetic rat model are changed and whether the neuroretinal apoptosis could be ameliorated by the administration of glial cell line–derived neurotrophic factor ( GDNF ). Methods Diabetes was induced by intraperitoneal injection of streptozotocin ( STZ ) in Sprague–Dawley rats. GLAST protein expression levels were determined by Western blotting, whereas apoptosis of retinal neurons was evaluated by TUNEL staining. To assess the role of GDNF in ameliorating the STZ ‐induced retinal changes, GDNF / GDNF with si RNA directed against GLAST was injected into the vitreous after STZ injection. Results In rat retinas 4 weeks after the onset of STZ ‐induced diabetes, TUNEL ‐positive cells were significantly increased, whereas GLAST levels were significantly reduced. Intraocular administration of GDNF at the early stage of diabetes remarkably increased the GLAST levels and decreased TUNEL ‐positive signals in the retinas. These effects of GDNF were largely abolished by coadministration of GLAST si RNA . Conclusions GDNF , administrated at the early stage of diabetes, could rescue retinal cells from neurodegeneration by upregulating the expression of GLAST .
机译：概述目的谷氨酸摄取功能障碍主要由谷氨酸-天冬氨酸转运蛋白（GLAST）介导，可能导致糖尿病性视网膜病变的视网膜细胞凋亡。这项研究的目的是研究如何改变糖尿病大鼠模型的神经细胞凋亡和GLAST的表达水平，以及是否可以通过给予神经胶质细胞源性神经营养因子（GDNF）改善神经视网膜的凋亡。方法腹腔注射链脲佐菌素（STZ）诱导Sprague–Dawley大鼠糖尿病。通过蛋白质印迹测定GLAST蛋白表达水平，而通过TUNEL染色评价视网膜神经元的凋亡。为了评估GDNF在改善STZ诱导的视网膜变化中的作用，在STZ注射后将GDNF / GDNF和针对GLAST的si RNA注入玻璃体。结果在STZ诱导的糖尿病发作4周后的大鼠视网膜中，TUNEL阳性细胞显着增加，而GLAST水平显着降低。在糖尿病早期眼内给予GDNF可以显着增加视网膜中的GLAST水平并降低TUNEL阳性信号。共同施用GLAST si RNA可以完全消除GDNF的这些作用。结论GDNF在糖尿病早期可以通过上调GLAST的表达来挽救视网膜细胞的神经变性。

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