摘要目的：探讨Fractalkine（CX3CL1）及其受体在5XFAD模型小鼠视网膜损伤黄斑变性机制中的作用。方法分别取6月龄5XFAD小鼠和6月龄野生型小鼠各12只。摘取眼球制作冷冻切片，使用淀粉样蛋白β（ Aβ）、CX3CL1和CX3CR1单克隆抗体行免疫荧光检测。使用CD11b和CD68单克隆抗体分别与CX3CR1抗体进行免疫荧光共表达研究以检测CX3CR1阳性细胞的来源。制备视网膜的总蛋白和总mRNA提取物，经逆转录-聚合酶链反应和Western blot检测视网膜中CX3CL1及其受体CX3CR1的mRNA和蛋白的表达。结果（1）与6月龄野生型小鼠相比，6月龄5XFAD小鼠的视网膜色素上皮细胞内有明显的Aβ沉积。（2）与6月龄野生型小鼠相比，6月龄5XFAD小鼠的视网膜中CX3CL1明显上调，CX3CL1主要表达于视网膜神经节细胞层；而其受体CX3CR1在视网膜神经节细胞层的表达也明显上调。（3）与6月龄野生型小鼠相比，6月龄5XFAD小鼠眼内CX3CL1和CX3CR1的蛋白和mRNA表达明显上调。（4）免疫荧光共表达结果显示CX3CR1与CD11b有显著的共表达，双阳性细胞集中于神经节细胞层；而CX3CR1与CD68无共表达。结论 Fractalkine及其受体可能与Aβ诱导的5XFAD小鼠视网膜损伤的炎症机制相关。

abstractsObjective To detect the expression and the function of Fractalkine( CX3CL1) and its receptor CX3CR1 in neurodegenerative changes of the retina.Methods Twelve 5XFAD mouse and twelve wild type mouse were enrolled. Frozen sections were prepared for histopathological tests.Immunofluorescence study for Amyloid β, CX3CL1 and CX3CR1 was carried out.Co-expression study for CX3CR1/CD11b or CX3CR1/CD68 was carried out.Total protein and total mRNA from the eyes of both 5XFAD and wild type mouse were extracted.The expression of mRNA and protein of CX3CL1 and CX3CR1 in the eyes were determined by reverse transcription-polymerase chain reaction ( RT-PCR) and Western blots test, respectively.Results In wild type mouse, both CX3CL1 and its receptor CX3CR1 can be detected in the retina with low expression, however there is no Amyloid βdepositions in retina.In 6 months 5XFAD mouse, an obvious up-regulated Amyloidβexpression can be seen in the RPE cells, and the number of both CX3CL1 and CX3CR1 positive cells has up-regulated in the ganglion cell layer of eyes accompanied with the increased expression of their mRNA and protein.The co-expression study showed that CX3CR1 co-expressed with CD11b, but not with CD68.Conclusion Fractalkine and its receptor play a role in Amyloid βinducing degenerative retinal inflammation in 5XFAD mouse.