急性高眼压对视网膜谷氨酸转运体GLAST表达影响

THE EFFECT OF ACUTE OCULAR HYPERTENSION ON GLUTAMATE TRANSPORTER GLAST EXPRESSION IN RETINA

目的探讨急性高眼压时视网膜谷氨酸转运体L-谷氨酸-L-天门冬氨酸转运体(GLAST)表达的变化。方法 Wistar大鼠20只,随机取一眼制作急性高眼压模型作为实验组,对侧眼行假手术作为对照组。分别于眼压升高后1、3、7、14d随机处死大鼠,每次5只,取大鼠视网膜,光镜下观察其形态学变化,用实时定量聚合酶链反应方法检测视网膜中GLAST mRNA的表达。结果光镜下,实验组急性高眼压损伤后1d,视网膜组织结构大致正常;3d时视网膜变薄,视网膜神经节细胞有所减少;7d时视网膜更薄,视网膜神经节细胞明显减少;14d时视网膜厚度变薄的更明显,细胞排列稀疏。实时定量聚合酶链反应显示,实验组GLAST mRNA表达在眼压升高后1d迅速上调,与对照组比较差异有显著性(t=3.267,P<0.05),3d时表达量下降(t=5.351,P<0.01),7d恢复至正常水平(t=2.013,P>0.05)。结论急性高眼压视网膜损伤的早期,视网膜谷氨酸转运体GLAST表达上调,可能与视网膜损伤中产生的过多的谷氨酸有关,可避免视网膜遭受谷氨酸的神经毒害作用。

Objective To study the changes of retina glutamate transporter GLAST following acute ocular hypertension（AOH）. Methods Twenty Wistar rats were involved in the present study.An AOH model was created in each random eye,and a sham surgery was done in the fellow eye served as a control.The rats were killed after elevation of intraocular pressure for one,three,seven and 14 days,with five rats of each time.Their retina samples were collected and the morphology was investigated by a light microscope.The expression of GLAST mRNA was detected by real time fluorescence quantitative RT-PCR. Results Microscopically,one day after AOH injury,the structure of the retina tissue was roughly normal;after three days,the retina became thinner with a decrease of retinal ganglion cells;after seven days,the thickness of retina showed more obviously thin,and the number of retinal ganglion cells decreased dramatically;after 14 days,further more thinner retina was seen with sparse align of the cells.The real time fluorescence quantitative RT-PCR showed,in the experimental group,the expression of GLAST mRNA was increased rapidly after one day of AOH,the difference being significant versus the control group（t=3.267,P〈0.05）,the expression declined on day 3（t=5.351,P〈0.01）,returned to normal level on day 7（t=2.013,P〉0.05）. Conclusion The up-regulation of expression of retina glutamate transporter GLAST in the early stage of AOH is probably related to redundant production of glutamic acid in the process of retinal damage.