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大鼠视网膜不完全性缺血引起细胞凋亡及bcl-2表达的研究

http://www.cnophol.com 2009-10-20 9:44:55 中华眼科在线

  大鼠视网膜不完全性缺血引起细胞凋亡及bcl-2表达的研究

  解剖科学进展 2000年第2期第6卷 原著

  作者:程欣 郑达人

  单位:程欣(暨南大学医学院组织学胚胎学教研室);郑达人(人体解剖学教研室 广州510632)

  关键词:视网膜;缺血;细胞凋亡;bcl-2

  摘 要:目的:通过结扎双侧颈总动脉造成大鼠视网膜不完全性缺血,用TUNEL及免疫组化方法观察视网膜细胞凋亡和bcl-2的表达。结果:缺血1天即见节细胞层和内核层出现凋亡细胞,7天在外核层也出现;高峰时间是缺血14天,术后60天仍可见凋亡细胞。缺血1天Mulle’s细胞内侧部bcl-2表达明显,7天着色区域扩大至Mulle’s细胞外侧部,14天阳性反应局限于Mulle’s细胞内侧部,并且着色明显,持续至缺血30天。缺血60天bcl-2表达明显减弱。结论:细胞凋亡参与视网膜缺血损伤,缺血后bcl-2表达增强是细胞防御功能增强的体现。

  The Cell Apoptosis and Bcl-2 Gene Expression in Incomplete Ischemic Retina in the Rat

  cheng Xin(Department of Histology %26 Embryology)

  zheng Daren(Department of Anatomy, Medical College, Jinan University, Guangzhou 510632)

  Abstract:Purpose: A model of 2VO, which can reduce the retinal blood flow, was used to give an ischemic insult to the rat retina. The apoptosis during the retinal ischemia was detected by tUNEL. Immunohistochemical technique as used for the localization of bcl-2 in retina. Results: The poptotic cells were present in INL and GCL on 1 day, and in ONL on 7 day. The peak of apoptotic cell’s numbers appeared on 14 day, and lasted 60 days postischemia. The expression of bcl-2 gene increased obviously on 1 day postischemia in the inner side cytoplasm of Muller’s cell, on 7 day, the positive staining extended into the outer side cytoplasm of Muller’s cell. On 14 day, it appeared that the bcl-2 positive staining was shown only in some cells in GCL and the inner side cytoplasm of Muller’s cell, namely those processes in GCL and endfeet, the positive staining in the outer side cytoplasm of Muller’s cell was not evident, and lasted 30 days. The bcl-2 immunoreactivity sharply dropped on 60 day. Conclusions: Appoptosis played an important role in ischemic cell loss. The increase in bcl-2 immunostaining of retina after ischmic insult implied the enhancement of defensive function.

  Keywords:retina; ischemia; apoptosis; bcl-2参考文献:

  [1]Buchi ER. Cell death in the rat retina after a pressure induced ischaemia-reperfusion insult, an electron microscopic study. Iganglion cell layer and inner nuclear layer. Exp Eye res, 1992,55, 605

  [2]夏潮涌,夏志坚.细胞核体积测量与计算的几种方法比较.中国作视学与图像分析,1997,2(4):226

  [3]Bogousslavsky J and Regli F. Cerebro-retinal ischemia after bilateral occlusion of internal carotid artery. A study with prospective follw up. neuroradio, 1985, 27: 238

  [4]Ekl6f B and Siesjo BK. The effect of bilateral carotid artery ligation upon the blood flow and the energy state of the rat brain.Acta Physiol Scand, 1972, 86:155

  [5]McKerracher L, Vidal-Sanz M, Essagian C, et al. Selective impairment of slow axonal transport after optic nerve injury in adult rats. J neuroscl, 1990, 10:2834

  [6]赵士福,蔡文琴,邓晓林等.大鼠脑缺血过程中神经细胞死亡的研究.解剖学报,1997,28(4):342

  [7]刘善荣,孟琳.大鼠暂时性全脑缺血再灌后海马区凋亡检测.解剖学杂志,1998,21(3):206

  [8]Li Y, Chopp M, Jiang N, et al. Induction of DNA fragmentation after 10 to 20 minutes of focal cerebral ischemia in rat. Stroke,1995, 26:1252

  [9]程欣,沈伟哉,郑达人.细胞调亡研究进展.解剖学杂志,1998,21 (4):368

  [10]Chen ST, Garey LJ and Jen LS. Bcl-2 proto-oncogene protein immunoreactivity in normally developing and axotomised rat retinas. Neurosci lett, 1994, 172: 11

  [11]Chen ST, Gentleman SM, Garey LJ, et al. Distribution of β- amyloid precursor and B-cell lymphoma protooncogene proteins in the rat retina after optic nerve transection or vascular lesion. J Neuropathology and Experimental Neurology, 1996, 55: 1073

  [12]Martinou JC, Dubois Dauphin M, Staple JK, et al. Overexpression of bcl-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia. Neuron, 1994,13: 1017

  [13]Kane DJ, Sarafian TA, Anton R, et al. bcl-2 inhibition of neural death: decreased generation of reactive oxygen species. Science, 1993, 262, 1274

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