GM-1对大鼠视网膜缺血再灌注损伤后NF-кB表达的影响

目的：观察神经节苷脂(monosialoganglioside，GM-1)对大鼠视网膜缺血再灌注损伤后视网膜结构的保护作用及对核因子-κB(nuclear factor-kappaB, NF-κB )表达的影响，探讨其可能的保护机制。方法：健康成年Wistar大鼠75只，随机分为3组：正常组5只、NS组35只、GM-1组35只。正常组不加任何处理因素，NS组和GM-1组通过升高眼压造成视网膜缺血60min，分别于缺血前12、1h及缺血结束时3次腹腔注射NS 3ml·kg-1或GM-1 3ml·kg-1，并于再灌注0(单纯缺血后)、1、6、12、24、72和168h共7个时点取双眼眼球，每时间点5只。HE染色观察视网膜组织结构并测量视网膜内层平均厚度(mean thickness of the inner retinal layers, MTIRL)，免疫组化SP法检测NF-κB的表达并计算阳性细胞率。方差分析法进行统计处理。结果：大鼠视网膜缺血再灌注后，内层视网膜相继出现水肿和萎缩。再灌注后大鼠视网膜内层NF-κB迅速激活，随后其表达逐渐下降。GM-1可明显减轻视网膜缺血再灌注后的组织损伤，并显著抑制NF-κB的活化。结论：NF-κB活化可能是视网膜缺血再灌注损伤的早期始动因素。GM-1对视网膜缺血再灌注损伤具有明确的保护作用，对NF-κB的抑制可能是其保护机制之一。

Effect of GM-1 on NF-kB in rat retinas after ischemia-reperfusion injury

Objective: To investigate the protective effect of monosialoganglioside GM-1 on rat retinal tissues and the influence of GM-1 on NF-κB after ischemia-reperfusion injury. Methods: Seventy-five healthy adult Wistar rats were randomly divided into 3 groups: the control group(n=5), the NS group(n=35) and the GM-1 group(n=35). The control group received no treatment. Rats in the other 2 groups received complete retinal ischemia by increasing the intraocular pressure for 60 minutes and they were intraperitonially injected to 3 ml·kg-1 NS or 3 ml·kg-1 GM-1 at 12 and 1 hour before and immediately after ischemia. According to the survival time after reperfusion, the experimental 2 groups were sub divided into 7 time points: 0 (only ischemia), 1, 6, 12, 24, 72 and 168 hours after ischemia. Morphological changes and mean thickness of the inner retinal layers (MTIRL) of the retina were determined under light microscopy. Expression of NF κB was determined by the immunohistochemistry method. Results: Rats inner retinas had the lesion process of edema and atrophy after ischemia reperfusion injury.gradually decreased. Pathological changes of retina and activation of NF κB were obviously relieved by GM-1. Conclusion: GM-1 definitely protects against retinal ischemia-reperfusion injury and it is a potential agent for retinal ischemia-reperfusion injury.