核转录因子-κB在大鼠视网膜缺血再灌注损伤中的表达

NF-κB expression in rat retinal ischemia-reperfusion injury

目的建立大鼠视网膜缺血再灌注(retinal ischemical reperfusion injury,RIRI)模型,观察不同程度损伤的视网膜组织病理改变,检测凋亡的存在,探讨核转录因子-κB(nuclear factor-kappa B,NF-κB)在大鼠RIRI中的表达。方法SD大鼠随机分为角膜损伤组和缺血再灌注组,分别建立角膜损伤模型和建立15kPa、60min高眼压视网膜缺血模型,光镜观察视网膜损伤后的组织病理改变,原位细胞凋亡检测,免疫组织化学检测NF-κB的表达情况。结果角膜损伤组视网膜无改变,缺血再灌注组出现组织病理改变,包括视网膜水肿,空泡变性,核固缩、溶解,结构紊乱等,随再灌注时间的延长,视网膜损害加重。原位细胞凋亡检测中,缺血再灌注组的凋亡细胞阳性表达均分布于神经节细胞层及内核层细胞,24h时表达最强。NF-κB在再灌注6h开始表达,24h表达最强。结论RIRI主要导致神经节细胞层及内核层细胞损伤,NF-κB的表达和凋亡可能是损伤的重要机制,且二者有着密切联系,表现出一致的规律性。

Objective To establish rat model of retinal ischemical reperfusion and observe the development process of retinal injury. To investigate apoptosis occur in retina and study NF-κB expression in rat retinal ischemia-reperfusion injury. Methods Sprague-Dawley rats were divided randomly into corneal injured group and ischemia-reperfusion group. Corneal injured model and 15 kPa,60 minutes pressure-induced ischemia reperfusion model were made respectively. Histopathological change was detected with light microscopy, apoptosis detection by terminal dUTP nick end labeling （TUNEL） and NF-κB examined in the retina by immunohistochemicy. Results Compared with corneal injured group, histopathological changes were found in ischemia-reperfusion group, including retinal edema, vacuolar degeneration, karyopyknosis and karyolysis,derangement of retinal constitution. Retinal injury became more serious with the reperfusion time. TUNEL positive expression was detected in inner nuclear layer and ganglio, cell layer,and the highest level of expression occurred at 24 hours after injury in iscnemia-reperfusion group. NF-κB began to express at 6 hours after ischemical reperfusion in ischemia-reperfusion group and the highest level of expression were occurred at 24 hours. Conclusion The damage of retinal ischemical reperfimion is mainly localized in inner nuclear layer and ganlion ceil layer. NF-κB expression and apoptosis are the important mechanism of the retinal disorder.