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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:

35卷

期数:

2015年1期

页码:

009-14

栏目:

实验研究

出版日期:

2015-01-05

文章信息/Info

Title:

Role of activated microglia in retinal ischemia-reper-fusion injury of rats

作者:

李娟娟; 李燕; 汤志伟

６５００３１　云南省昆明市，昆明医科大学第一附属医院眼科

Author(s):

LI Juan-Juan ;  LI Yan ;  TANG Zhi-Wei

Department of Ophthalmology, the First Affiliated Ho.spital of Kunming Medical University , Kunming 650031, Yunnan Province , China

关键词:

视网膜小胶质细胞; 缺血再灌注损伤; CD68; 电镜; 免疫组织化学

Keywords:

retinal microglia ;  ischemia-reperfusion injury ;  CD68 ;  electron microscope ;  immunohistochemistry

DOI:

10.13389/j.cnki.rao.2015.0003

文献标志码:

A

摘要:

目的　探讨活化的小胶质细胞在视网膜缺血再灌注损伤过程中的作用。方法　前房灌注法建立视网膜缺血再灌注动物模型，在损伤发生后２ｈ、１２ｈ、２４ｈ、４８ｈ、７２ｈ，采用免疫组织化学染色方法检测特异性抗原标志物ＣＤ６８的表达，观察活化小胶质细胞的分布、活化程度等，同时观察相应时间点的视网膜超微结构变化。结果　对照组中视网膜小胶质细胞主要位于神经节细胞层。缺血再灌注损伤后２ｈ组视网膜小胶质细胞的分布部位、表达量等基本与对照组相同；缺血再灌注损伤后１２ｈ组视网膜中ＣＤ６８＋细胞表达增多，内丛状层可见阳性细胞。缺血再灌注损伤后２４ｈ组ＣＤ６８＋细胞表达明显增多，部分向视网膜外层迁移。缺血再灌注损伤后４８ｈ组进入视网膜外层的ＣＤ６８＋细胞多数出现于视网膜内丛状层、内核层、外丛状层。缺血再灌注损伤后７２ｈ组活化小胶质细胞数量达到最高水平。视网膜超微结构显示：缺血再灌注损伤后１２ｈ组开始出现损伤表现，视网膜神经节细胞间隙扩大、光感受器细胞外节膜盘疏松变形、可见散在小胶质细胞；缺血再灌注损伤后２４ｈ组病变继续加重，小胶质细胞数量明显增多；缺血再灌注损伤后７２ｈ组病变继续加重，视网膜神经节细胞数量明显减少，细胞核膜肿胀溶解，细胞器溶解，大鼠视网膜神经节细胞层内可见凋亡小体、小胶质细胞，证明了小胶质细胞对光感受器的损伤作用。结论　视网膜缺血再灌注损伤出现明显小胶质细胞活化，活化的小胶质细胞在视网膜超微结构的损伤中发挥着重要作用。

Abstract:

Objective To discuss the role of activated microglia in retinal ischemia-reperfusion injury. Methods Retinal ischemia reperfusion animal model was established by anterior chamber perfusion .immunohistochemical staining was used to detect the expression of CD68 after 2 hours , 12 hours .24 hours.48 hours ,72 hours of the injury,the distribution and activated degree of activated microglia were observed, and the retinal ultrastructure was also observed. Results The microglia were mainly located in the ganglion cell layer in normal control group. In the group of 2 hours after injury,the distribution and the expression of the microglia were similar with the normal control group. In the group of 12 hours after injury, the number of CD68+ cells increased,positive cells could be observed in the inner plexiform layer. In the group of 24 hours after injury, CD68 + cells were significantly increased and migrated to the outer retina. In the group of 48 hours after injury ,CD68 + cells could be observed in the inner nuclear layer, outer plexiform layer of the retina. In the group of 72 hours after injury, the number of activated microglia reached the highest level. Ultrastructure damage began to appear after 12 hours of the injury , the gap between the retinal ganglion cells expanded , the outer segment membrane of the photoreceptor became loose . some nucroglia could be observed;ln the group of 24 hours after injury , the gap between the retinal ganglion cells continued to expand and the number reduced. the outer segment membrane of photoreceptor deformed, fractured. swelled, the number of microglia significantly increased. In the group of 72 hours after injury , the lesions continued to increase. the number of retinal ganglion cells significantly reduced,membrane swelled and organelles dissolved. The apoptotic bodies could be observed in the layer of retinal ganglion cells,phagosome in the microglia was a direct proof of the damage of the microglia to light receptors. Conclusion The activated microglia appears in the retinal ischemia-reperfusion injury , which shows that the activated microglia plays an important role in the retinal ultrastructure.

备注/Memo

备注/Memo:

国家自然科学基金资助（编号：８１３６０２０４）

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更新日期/Last Update: 2015-01-04