视网膜缺血再灌注损伤中WTp53蛋白、CyclinD1表达的研究及bFGF对其的影响

目的探讨碱性成纤维细胞生长因子(bFGF)在大鼠视网膜缺血再灌注损伤(RIRI)中的治疗作用及机制。方法将28只Wistar大鼠随机分为正常组、缺血组和bFGF治疗组,其中后两组又按再灌注时间不同分为再灌注后1、6、12、24、48和72h6个时间段。通过前房穿刺加压法制作成RIRI动物模型,并在以bFGF(治疗组)或平衡盐溶液(缺血组)玻璃体腔注射后按不同时段处死动物,通过免疫组织化学链酶卵白素-生物素复合体(SABC)法检测各时段视网膜组织中野生型p53蛋白(WTp53)和细胞周期蛋白D1(CyclinD1)的表达变化。结果缺血组视网膜在再灌注后6h可发现有WTp53蛋白及CyclinD1的表达,24h达到高峰,48h仍持续强表达,72h表达已明显下降;bFGF治疗组各观察指标变化规律基本与缺血组相似,但表达量相对明显减弱,两组比较,在再灌注6-48h时段差别P值均<0.05,具有统计学意义。结论bFGF可抑制RIRI时WTp53蛋白和CyclinD1在视网膜表达的增高。

Expression of WTp53 and Cyclin D1 in rat retina with ischemia/reperfusion injury and after bFGF treatment

Objective To investigate the therapeutic effect of basic fibroblast growth factor (bFGF) on retina ischemia/ reperfusion injury and its mechanisms. Methods The model of retina ischemia/reperfusion injury was made in the left eyes of 24 rats by increasing the intraocular pressure, and the right eyes of experimental rats were as the treatment group and other 4 rats was normal control group. bFGF or balanced saline solution were intravitreously injected at the 1st,6th, 12nd ,24th ,48th and 72nd hour in the treatment group and model group, respectively. The expressions of wide type p53( WTp53) protein and Cyclin Dl were determined by strept-avidin-biotin complex ( SABC ) immunohistochemistry. Results WTp53 protein and CyclinDl were expressed at the 6th hour after reperfusion in the ganglion cell layer, nerve fiber layer and inner nuclear layer and reached peak at the 24th hour,and then the expressions were obviously decreased at the 72nd hour in the model group. In treatment group, the expressions and changes of WTp53 and GyclinD1 were similar to those in the model group,but there was a decrease of expression amount with statistical significance at the 6th, 12nd, 24th and 48th hour after reperfusion between the ischemia group and treatment group ( P < 0. 05 ) . Conclusion WTp53 protein and Cyclin Dl may be involved in the mechanisms of retina ischemia/reperfusion injury and cells apoptosis, and bFGF can inhibit this procedure.