摘要
目的 探讨 Fas/ Fas L在大鼠视网膜缺血再灌注损伤中的表达与细胞凋亡的关系及碱性成纤维细胞生长因子 ( basic fibroblastgrowth factor b FGF )的治疗作用。 方法 前房加压法制作大鼠视网膜缺血再灌注损伤模型 ,2 8只大鼠随机分为正常组和手术组 ,其中手术组大鼠左眼为缺血再灌注组 ,右眼为治疗组 (玻璃体腔内注射 b FGF) ,手术组又按照再灌注后不同时间段分为 1、6、12、2 4、48、72 h组。应用末端脱氧核酸转移酶介导的脱氧三磷酸尿苷缺口末端标记 ( terminal deoxynucleotidyl transferase- mediated d UTP-biotinnick- end,TUNEL )法检测视网膜神经细胞凋亡指数 ( apoptosis index,AI) ,免疫组织化学法检测视网膜组织中 Fas、Fas L的表达。 结果 视网膜神经细胞的凋亡出现于再灌注后 6 h,并逐渐递增 ,2 4h达到高峰 ,48h开始下降 ,72 h组不明显。 Fas、Fas L表达改变与凋亡的神经细胞改变基本一致。 b FGF治疗组各观察指标表达变化规律与缺血组基本一致 ,但 AI值在 12、2 4、48h组明显低于缺血组 ( P<0 .0 5 ) ;Fas表达在6、12、2 4h组较缺血组显著下降 ( P<0 .0 5 ) ;Fas L表达在 12、2 4、48h组较缺血组明显下降 ( P<0 .0 5 )。 结论 Fas/ Fas L死亡诱导系统参与视网膜缺血再灌注损伤 。
Objctive To explore the relationship between the expression of Fas/FasL and the apoptosis occurs in retinal ischemia/reperfusion injury of rats, as well as the therapeutic effects of bFGF on the ischemic retina. Methods The models of retinal ischemia/reperfusion injury was made by transient elevating introcular pressure. A total of 28 rats were divided into normal and operation group.The latter were subdivided into 1 hour, 6, 12, 24, 48 and 72 hours after reperfusion group, in which the left eyes of the rats were in the ischemia/reperfusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of Fas and Fas ligand was studied by strept avidin-biotin complex (SABC)immunohistochemistry. Results No positive cells were observed in the normal rats′ retinae, but there was a significant number of TUNEL positive cells in 6-24 hours after transient ischemia followed by a decrease at the 48th hour. The number of TUNEL positive cells reached a maximum at the 24th hour after ischemia. The expression of Fas gradually increased as early as when it was at the 6th hour, reached a peak at the 24th hour, and then decreased at the 48th hour. Similarly, the expression of Fas ligand was at peak in 24-48 hours in GCL and INL of retina. Conclusions Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retina. Fas/FasL may play an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through downregulation of the expression of Fas/FasL and may represent an important mechanism for therapeutic neuroprotection.
出处
《中华眼底病杂志》
CAS
CSCD
2003年第3期160-163,共4页
Chinese Journal of Ocular Fundus Diseases
基金
山东省教委基金资助项目 (J0 0 K53)
