Elucidation of the role of ER stress in neuronal abnormalities of diabetic retinopathy

我们已经证明，在糖尿病应激下培养的大鼠视网膜中，caspase依赖的细胞死亡途径与神经元细胞死亡相关。此外，我们已经表明，ER应激相关的细胞死亡途径与培养的糖尿病大鼠视网膜和人类糖尿病视网膜中的神经元细胞死亡有关。总之，我们的研究结果表明，在糖尿病视网膜线粒体和ER应激细胞死亡途径之间存在分子串扰。此外，BDNF，NT-4和胞二磷胆碱拯救神经元细胞死亡，并诱导神经突起再生培养的糖尿病大鼠视网膜。尤其是NT-4对糖尿病视网膜损伤的神经元具有最强的保护和再生作用。

We have demonstrated that mitochondria-caspase dependent cell death pathways are associated with neuronal cell death in cultured rat retinas under diabetic stress. In addition, we have suggested that ER stress-related cell death pathways are related to neuronal cell death in cultured diabetic rat retinas and in human diabetic retinas. Taken together, our results indicate that there are a molecular crosstalk between mitochondria and ER stress cell death pathways in diabetic retinas. Furthermore, BDNF, NT-4 and citicoline rescued neuronal cell death and induce neurite regeneration in cultured diabetic rat retinas. Especially NT-4 showed the most neuroprotective and regenerative effect in damaged retinal neurons of diabetic retinas.