期刊文献+

碱性成纤维细胞生长因子对视网膜缺血再灌注损伤中凋亡相关基因表达的影响 被引量:10

Effect of basic fibroblast growth factor on expression of apoptosis-related genes in retinal ischemia-reperfusion injury
原文传递
导出
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)
关键词 成纤维细胞生长因子 碱性 再灌注损伤 视网膜 基因表达 Fibroblast growth factor,basic Reperfusion injury Retina Gene expression
  • 相关文献

参考文献13

二级参考文献18

  • 1Bethel A, Kirsch JR, Koehler RC, et al. Intravenous basic fibroblast growth factor decreases brain injury resulting from focal ischemia in cats. Stroke, 1997,28 : 609-615. 被引量:1
  • 2Buchi ER. Cell death in the rat retina after a pressureinduced ischaemia-reperfusion insult: an electron microscopic study. I.Ganglion cell layer and inner nuclear layer. Exp Eye Res, 1992,55:605-613. 被引量:1
  • 3Kaneda K, Kashii S, Kurosawa T, et al. Apoptotic DNA fragmentation and upregulation of Bax induced by transient ischemia of the rat retina. Brain Res, 1999,815 : 11-20. 被引量:1
  • 4Nagata S, Golstein P. The Fas death factor. Science, 1995, 267:1449-1564. 被引量:1
  • 5Griffith TS, Brunner T, Fletcher SM, et al. Fas ligand-induced apoptosis as a mechanism of immune privilege. Science, 1995, 270:1189-1192. 被引量:1
  • 6Rosenbaum DM, Gupta G, D'Amore J, et al. Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia. J Neurosci Res, 2000,61 .. 686-692. 被引量:1
  • 7Yue TL, Ma XL, Wang X,et al. Possible involvement of stress-activated protein kinase signalling pathway and Fas receptor expression in prevention of ischemia/reperfusion-induced cardiomyocyte apoptosis by carvedilol. Circ Res, 1998,82 : 166-174. 被引量:1
  • 8Chang M W,Science,1995年,267卷,518页 被引量:1
  • 9卢圣栋,现代分子生物学实验技术,1993年,315页 被引量:1
  • 10鄂征,组织培养技术(第2版),1988年,176页 被引量:1

共引文献54

同被引文献110

引证文献10

二级引证文献36

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部