基础医学与临床 ›› 2013, Vol. 33 ›› Issue (2): 133-138.

• 研究论文 • 上一篇    下一篇

Müller细胞反应性胶质化在急性高眼压致大鼠视网膜损伤中作用

苏吉儿1,丁静文2,韩松3,罗宏3,李俊发1   

  1. 1. 首都医科大学
    2. 首都医科大学附属北京同仁医院
    3. 首都医科大学神经生物学系
  • 收稿日期:2012-07-16 修回日期:2012-11-30 出版日期:2013-02-05 发布日期:2013-01-25
  • 通讯作者: 李俊发 E-mail:junfali@ccmu.edu.cn
  • 基金资助:
    胞质NPM突变蛋白调控TRAF6介导的AKT泛素化激活在急性髓系白血病中的作用;胞质NPM突变蛋白调控TRAF6介导的AKT泛素化激活在急性髓系白血病中的作用;国家自然科学基金;胞质NPM突变蛋白调控TRAF6介导的AKT泛素化激活在急性髓系白血病中的作用;北京市属高等学校人才强教深化计划创新人才资助;教育部高等学校博士点科研基金

Role of Müller cell-specific reactive gliosis in acute ocular hypertension-induced retinal damage of rats

  • Received:2012-07-16 Revised:2012-11-30 Online:2013-02-05 Published:2013-01-25
  • Contact: Jun-fa LI E-mail:junfali@ccmu.edu.cn

摘要: 目的 观察Müller细胞反应性胶质化在急性高眼压(AOH)大鼠视网膜中变化及其抑制对视网膜损伤的影响。方法 建立大鼠AOH青光眼模型,分为正常对照(Ctrl)、AOH和AOH+玻璃体内注射胶质毒素α-氨基己二酸(AAA)后再灌注1、3和5d组,以及单纯AAA和AOH+PBS对照组。TUNEL染色检测细胞凋亡,GFAP免疫荧光染色反应Müller细胞反应性胶质化程度,Thy-1染色标记视网膜神经节细胞(RGCs)。结果 AOH可致大鼠视网膜内丛状层和内核层明显变薄、神经节细胞层内细胞排列紊乱和数量减少,并诱发Müller细胞反应性胶质化(GFAP表达增加)。同时,AAA抑制Müller细胞反应性胶质化可明显缓解AOH所致RGCs丢失和凋亡发生。结论 Müller细胞反应性胶质化参与AOH所致视网膜损伤,抑制其反应性胶质化可能是改善高眼压性青光眼视网膜病变的一种有效治疗方法。

关键词: 急性高眼压, 视网膜, Müller细胞, 视网膜神经节细胞

Abstract: Objective To observe Müller cell-specific reactive gliosis in rat retina following acute ocular hypertension (AOH) and its effect on AOH-induced retinal damage. Methods The AOH rat model was established, and animals were divided into control (Ctrl), AOH and AOH+α-aminoadipic acid (AAA, intravitreal injection) treated groups (1, 3 and 5d subgroups according the reperfusion time), and AAA treatment or AOH+PBS control group. TUNEL assay was used to detect cell apoptosis, GFAP immunofluorescent staining was performed to respond Müller cell-specific reactive gliosis, and Thy-1 staining was applied to mark retinal ganglion cells (RGCs). Results AOH could attenuate the thicknesses of inner plexiform layer (IPL) and inner nuclear layer (INL), and cause cell disorganization and cell loss in ganglion cell layer (GCL) as well as the Müller cell-specific reactive gliosis (enhanced GFAP-immunoreactivity) in rat retina. In addition, we found that the inhibition of Müller cell-specific reactive gliosis by AAA intravitreal injection could significantly relief RGCs loss and cell apoptosis in GCL layer of AOH rat retina. Conclusion Müller cell-specific reactive gliosis was involved in AOH-induced retinal damage and its inhibition may be an effective therapeutic strategy for improving glaucomatous retinopathy.

Key words: acute ocular hypertension, retina, Müller cells, retinal ganglion cells

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