小鼠视网膜缺血-再灌注后核因子-κB的激活

Activation of NF-κB in the mouse retina after ischemia reperfusion

目的 研究小鼠视网膜缺血 再灌注所致视网膜神经细胞凋亡中 ,核因子 κB的表达。方法 通过升高小鼠眼内压造成视网膜缺血 ,用计算机图像分析方法测量视网膜再灌注后神经细胞凋亡的比例和视网膜厚度的改变。免疫组化标记核因子 κBp6 5亚单位 ,并与原位缺口末端标记(TUNEL)做双重荧光标记 ,分析核因子 κB的表达与细胞凋亡之间的时相关系。结果 视网膜缺血 再灌注后最初 2 4h ,视网膜内层厚度增加 ,至 16 8h ,厚度显著减少。再灌注后 6h ,神经节细胞和内核细胞层中p6 5的免疫表达增强 ,至 2 4h达到高峰 ,这一过程与TUNEL标记的时相一致。结论 视网膜缺血 再灌注损伤后 ,核因子 κB的激活对于视网膜神经细胞的凋亡有重要作用 ,对于其起促进凋亡还是起抑制凋亡的作用 ,则有待于进一步研究。

Objective To investigate the expression of NF-κB following retinal ischemia and reperfusion injury in mice. Methods Retinal ischemia was induced by elevation of intraocular pressure. Retinal degeneration and atrophy were quantified by an image analysis system. Immunohistochemistry using p65 monoclonal antibody was performed on the retina and co-related with TUNEL labeling. Results Inner retinal thickness was increased in the initial 24 hours following retinal ischemia and was ascribed to tissue edema, but was significantly decreased by 168 hours after reperfusion. Six hours after retinal ischemia, p65 immunoreactivity was increased in the ganglion cell and the inner nuclear layers, reached a peak at 24 hours, and was parallel to TUNEL labeling. Double labeling with p65 and TUNEL showed partial co-localization of p65 and TUNEL labeling, predominantly in the inner nuclear layer. Conclusions Activation of NF-κB appears to play an important role in retinal degeneration following retinal ischemia and reperfusion injury. The pro- and anti- apoptotic effects of NF-κB after retinal ischemia are being further investigated.