摘要
目的探讨碱性成纤维细胞生长因子(bFGF)对视网膜缺血再灌注损伤(RIRI)中凋亡相关基因表达的影响. 方法将28只Wistar大鼠随机分为正常组、缺血组和治疗组,其中后两组又按照不同再灌注时间分为再灌注后1、6、12、24、48、72 h 6个时间段.建立RIRI动物模型,以bFGF(治疗组)或平衡盐溶液(缺血组)玻璃体腔注射,通过免疫组织化学链酶卵白素-生物素复合体法检测不同时段视网膜组织中野生型(WT)p53、c-fos、c-jun基因的表达变化. 结果缺血组视网膜再灌注后6 h可发现有WTp53、c-fos和c-jun蛋白的表达,24 h达到高峰,48 h仍持续强表达,72 h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.二组比较,在再灌注6~48 h各时段差异有统计学意义(P<0.05). 结论 RIRI能引起WTp53、c-fos、c-jun基因在视网膜神经节细胞层与内核层表达的增高;WTp53、c-fos、c-jun基因可能通过在与RIRI的细胞凋亡中起作用而参与了RIRI的发生机制;bFGF可以抑制RIRI时WTp53、c-fos、c-jun基因在视网膜表达的增高,从而对RIRI起治疗作用.
Objective To investigate the effect of basic fibroblast growth factor (bFGF) on expression of apoptosis-related genes in retinal ischemia reperfusion injury (RIRI). Methods Twentyeight rats were divided into normal, ischernia and treatment group randomly; and the latter two groups were subdivided into 6 subgroups according to different time points: 1 hour, 6, 12, 24, 48, and 72 hours after reperfusion. The rats' model of experimental RIRI was established. After intravitreously injected with bFGF (treatment group) or balanced saline solution (ischemia group), the expressions of wide type p53 (WTp53),c-fos, and c-jun in each subgroups were detected by strept-avidin-biotin complex of immunohistochemistry. Result In ischemia group, the expression of WTp53,c-fos and c-jun was found 6 hours after reperfusion, reached the peak at the 24th hour after reperfusion, kept expressing strongly at the 48th hour, and decreased obviously at the 72nd hour. In treatment group, the rule of changes of expression of WTp53, c-fos and c-jun was similar to which in ischemia group, except that the expression amount was obvious decreased. There was statistical significance of the expression of WTp53, c-fos and c- jun between the ischemia and treatment group 6-48 hours after reperfusion (P〈0. 05). Conclusion The expression of WTp53, c-los, and c jun in retinal ganglion cell layer and inner nuclear layer may increase led by RIRI;WTp53,c-fos,and c-jun may be involved in the generant mechanisms of RIRI by playing parts in apoptosis ;bFGF can inhibit the increase of expression of WTp53 ,c-fos ,and c-jun in RIRI. Thus, which may has therapeutic effect on RIRI.
出处
《中华眼底病杂志》
CAS
CSCD
北大核心
2005年第5期310-313,共4页
Chinese Journal of Ocular Fundus Diseases
基金
山东省教育委员会基金资助项目(JOOK53)