目的 探讨大黄素对视网膜缺血再灌注损伤后视网膜神经节细胞(RGC)密度的影响.方法 通过前房灌注法使眼内压升高,建立大鼠视网膜缺血再灌注损伤模型.将36只SD大鼠随机分为正常对照组、损伤后未注射药物组(IR组)、注射对照液干预组(IR+DMSO组)和注射大黄素干预组(IR+Emodin组),其中IR组根据损伤后时间不同分为损伤1、2、3周组(IR1w组、IR2w组、IR3w组),每组6只.IR+DMSO组与IR+Emodin组在缺血再灌注损伤后第3、9、15天玻璃体腔分别注射DMSO和蛋白激酶2(CK2)抑制剂大黄素.3周后采用逆行荧光金染色和免疫组织化学染色方法标记RGC,计数各组RGC密度,行统计学分析.结果 IR2w、IR3w组与正常对照组比较,RGC密度明显减少(分别为P＜0.01和P＜0.001).IR +DMSO组与IR3w组比较,RGC密度的差异无统计学意义(P＞0.05).IR+Emodin组与IR3w组比较,RGC存活密度明显增多(P＜ 0.001).结论 缺血再灌注损伤后RGC密度随缺血再灌注时间延长而逐渐减少,CK2抑制剂大黄素在视网膜缺血再灌注损伤过程中对RGC有保护作用,提示CK2参与了RGC损伤的过程.%Objective To study the effects of casein kinase 2 (CK2) on retinal ganglion cells of rats subjected to ischemia reperfusion injury by 6-methyl-1, 3,8-trihydroxyanthraquinone (Emodin). Methods A total of 36 SD rats were used in this study. The ischemia reperfusion (IR) model was established by using anterior chamber cannulation to elevate IOP above systolic pressure for 75 minutes. To study the time-course of RGC death,the densities of RGC were examined at 1 week,2 weeks and 3 weeks after ischemia reperfusion injury,respectively. Rats in IR+DMSO group and IR+Emodin group received three times of intravitreal injection of DMSO or Emodin on days 3,9,15 after injury. Fluorogold and immunochemical staining were used to label the viable RGC. The densities of viable RGC were assessed 3 weeks after the injury. Results A significant loss of RGC was found in IR2w and IR3w group compared with the control group (P < 0.01 and P < 0.001). No significant RGC loss was observed between the IR+DMSO group and the IR3w group (P > 0.05). The density of RGC in IR+ Emdoin group significantly increased compared to the IR3w group (P < 0.001). Conclusion The inhibition of CK2 leads to protection of RGC. CK2 is involved in the injury of RGC after ischemia reperfusion injury. Our finding provides an impetus for study of the mechanism of RGC survival regulated by CK2 inhibition.
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