中文摘要：

目的研究信号转导与转录因子6（STAT6）基因敲除小鼠在视网膜急性缺血-再灌注损伤后视网膜神经节细胞（RGCs）的损伤情况及视网膜胶质纤维酸性蛋白（GFAP）的表达变化。方法野生型C57BL/6小鼠和STAT6基因敲除小鼠各8只,右眼制作急性缺血-再灌注损伤模型,左眼不做任何处理为对照组。急性缺血-再灌注损伤模型采用前房穿刺后生理盐水灌注法,液面高度保持约1.6m相当于眼压120mmHg,维持1h后拔出,再灌注48h后取眼球制作视网膜石蜡切片。TUNEL染色观察2种小鼠RGCs的凋亡,免疫荧光染色法观察视网膜GFAP的表达。结果急性缺血-再灌注损伤48h后,STAT6基因敲除小鼠RGCs的凋亡明显少于野生型C57BL/6小鼠。野生型小鼠损伤后视网膜内GFAP的表达较对照组明显增强,呈纤维样,排列呈栅栏状,由RGCs层贯穿至外核层,而STAT6基因敲除小鼠的GFAP表达增强不明显。结论 STAT6基因敲除对损伤后的RGCs有一定的保护作用,其保护作用有可能是通过降低胶质细胞的反应实现的。

英文摘要：

Background Immunological abnormality has been proposed as a contributing factor in the etiology of glaucomatous optic neuropathy.Cytokines are the hormonal factors that mediate many biological effects in both the immune and non-immune systems.STAT6-knock out （-/-） mice lack most functions associated with IL-4,resulting in the fail to produce Th2 CD4＋ T cells.Objective The aim of this study was to explore the retinal ganglion cell survival and glial fibrillary acidic protein GFAP expression in transient retinal ischemia-induced wide type mice and STAT6-knock out （-/-） mice.Methods The animal models of ischemia/reperfusion injury were established by perfusing the normal saline solution in the anterior chamber from the container with the height of 1.6 meters to elevate the intraocular pressure （IOP） to about 120 mmHg for 1 hour in the right eyes of 8 C57BL/6 mice and 8 STAT6 （-/-） mice.The left eye of mice were used as controls.The animals were killed and the eyeballs were enucleated at 48 hours after establishment of ischemia/reperfusion injury models.TUNEL assay was performed to identify the apoptosis of retinal ganglion cells （RGCs）.GFAP immunolabeling in Mller cells was detected by immunohistochemistry.The experimental procedure followed the Standard of Association for Research in Vision and Ophthalmology.Results TUNEL positive cells were detected mainly in retinal ganglion cell layer,showing the red fluorescence under the fluorescence microscope.Much more apoptotic cells were detected in the ischemic retinas of C57BL/6 mice than STAT6 （-/-） mice in 48 hours after transient ischemia.In the ischemic retina of C57BL/6 mice,there was a significant enhance in the expression of GFAP in the end feet and fibers of the Mller cells throughout the whole retina.But the expression of GFAP in retina of STAT6 （-/-） mice was much less in comparison with C57BL/6 mice in 48 hours after transient retinal ischemia.Conclusion Survival of retinal ganglion cells increases and expression of GFAP dec