目前研究证实视网膜色素上皮（RPE）细胞氧化损伤最终导致光感受器细胞变性凋亡在遗传性视网膜疾病发病中起主导作用，但是在遗传基因突变的情况下，氧化损伤如何导致遗传性视网膜疾病光感受器细胞变性凋亡的分子机制尚未明了。我们前期发现短波长光照射对遗传性视网膜动物模型损伤比正常小鼠要严重得多；同时我们在遗传性视网膜动物模型rd12小鼠基因治疗过程中又发现未经治疗的rd12小鼠视网膜上过氧化物酶6（Peroxiredoxin 6，PRDX6）表达上调，但是其具体抗氧化机制不明。本课题拟在前期研究基础上，通过基因调控、PCR、western blot、流式细胞技术、双重免疫荧光定位染色等方法，从分子-细胞-动物水平分析PRDX6在RPE细胞氧化损伤过程中的机制，探讨其在遗传性视网膜疾病发展中的作用。本研究结果可能为发现遗传性视网膜疾病的新分子标记和开展特异性靶向干预提供新策略。

In recent studies, the photoreceptor cell degeneration and apoptosis caused by the retinal pigment epithelium (RPE) cells oxidative injury were confirmed to play a important role in the pathogenesis of hereditary retinal diseases .But,in the case of genetic mutations, it is not clear that the molecular mechanisms of oxidative damage lead to photoreceptor cell apoptosis of hereditary retinal diseases. In previous study,we discovered short wavelength light caused much more serious retina injury in hereditary retinal disease mice model than in normal mice.we also found increased expression of peroxiredoxin 6 (PRDX6) in untreated retina of rd12 hereditary retinal disease mice in the process of gene therapy , but explicit antioxidant mechanism of PRDX6 is largely unknown.Based on previous finding, in this project, we will investigate regulation mechanism of PRDX6 protecting RPE cells oxidative injury in vitro and vivo via gene regulation strategy, PCR, western blot,flow cytometry, double- Immunofluorescence assay,etc. Furthermore, we will determine the function of PRDX6 in hereditary retinal disease mice. This study result may find new molecular markers and provide a new strategy to develop specific-target intervention to hereditary retinal diseases.