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

  • 1Muller A, Pietri S, Villain M, et al. Free radicals in rabbit retinaunder ocular hyperpressure and functional consequences. Exp Eye Res, 1997, 64; 637-643.
  • 2Cuevas P, Carcel[er F, ()rtega SN, et al. Hypotensive activity of fibroblast growth factor. Science, 1991, 254; 1208-1210.
  • 3牛膺筠,张瑞,周占宇,王红云,刘夫玲.碱性成纤维细胞生长因子对鼠视网膜缺血再灌注损伤的治疗作用[J].中华眼科杂志,2002,38(9):530-534. 被引量:34
  • 4Buchi ER. Cell death in rat retina after a pressure-induced ischemia-reperfusion insult: an electron microscopic study. I.Ganglion cell layer and inner nuclear layer. Exp Eye Res, 1992,55: 605-613.
  • 5Kuroiwa S, Katai N, Yoshimura N. A Possible Role for P16INK4 in Neuronal Cell Death after Retinal Isehemia-reperfusion Iniury.Invest Ophthalmol Vis Sei, 1998,39:610-617.
  • 6Wood K, Youle R, The role of free radicals and P53 in neuron apoptosis in vivo. Neurosci,1995,15;5851-5857.
  • 7La Feria F, Hall C, NgoI., et al. Extracellular deposition of amyloid upon P53-dependent neuronal cell death in transgenic mice. Clin Invest, 1996, 98:1626-1632.
  • 8蒋雷,夏永静,黎健.野生型p^(53)基因导入对培养的兔血管平滑肌细胞生长的抑制作用[J].中华心血管病杂志,1997,25(4):301-304. 被引量:13
  • 9国汉邦,黎健,董军,王抒.野生型p53基因导入诱导神经细胞凋亡[J].中国神经免疫学和神经病学杂志,2002,9(1):29-31. 被引量:6
  • 10Smeyne R, Vendrell M, Hayward M, et al, Continu-ousc-fos expression precedes programmed cell death in vivo. Nature, 1993,363; 166-169.

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.
  • 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.
  • 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.
  • 4Nagata S, Golstein P. The Fas death factor. Science, 1995, 267:1449-1564.
  • 5Griffith TS, Brunner T, Fletcher SM, et al. Fas ligand-induced apoptosis as a mechanism of immune privilege. Science, 1995, 270:1189-1192.
  • 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.
  • 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.
  • 8Chang M W,Science,1995年,267卷,518页
  • 9卢圣栋,现代分子生物学实验技术,1993年,315页
  • 10鄂征,组织培养技术(第2版),1988年,176页

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