23PEDF阳性视网膜神经节细胞计数及其变化规律G1 h,G12 h视网膜PEDF阳性的RGCs的数量没有明显变化(P005),1 d后开始增加(P005),到7 d达到高峰并维持在这个水平到28 d(P005),而C组自始至终没有明显变化 (P005, Tab 2).
表2各组PEDF阳性视网膜神经节细胞计数 略
3讨论
青光眼是一类以病理性眼压升高,生理凹陷扩大,视野损害为特点的疾病.它的发病机制、发展过程及有效治疗手段等诸多问题目前仍在讨论之中.近年来,随着对青光眼认识的不断深入,视网膜视神经损害的病理过程、病理机制和视神经保护的研究越来越受到重视,而高眼压是青光眼发生和发展的一个主要因素,因此建立长期稳定的高眼压动物模型是至关重要的一环,我们用巩膜浅层静脉烧烙法建立了长期稳定的EIOP模型[1].
PEDF是1989年由TombranTink[2]在培养的人胎儿视网膜色素上皮(retinal pigment epithelium,RPE)细胞的基质中发现一种独特的、相对分子质量为50 ku的蛋白质,氨基酸序列显示它是丝氨酸蛋白酶抑制超基因家族(serpins)的一员[3].已证实PEDF是一类神经营养因子[4],它能促进神经元的存活和分化[5,6];特异性地保护神经元免受凋亡及H2O2、谷氨酸等的毒性作用[711].但PEDF与慢性高眼压视网膜的关系的报道中仍较少见.
我们发现在正常情况下大鼠视网膜有PEDF表达,并且在不同细胞层的表达有所不同,这与国外报道的PEDF在正常猴眼中表达[12]的结果相似.EIOP的视神经损伤是随着时间的延长而逐渐加重的,大鼠EIOP模型建立后1 d眼压开始稳定并维持在40 kPa以上,而我们的实验结果也是在术后1 d,PEDF的表达开始增高,并呈现出递增趋势,到7 d达到高峰,且稳定在这个范围内到28 d之后,这与眼压的变化相一致.由此可以推测,眼压与PEDF在视网膜表达的增加有一定的关系.PEDF表达的增加主要分布在RGC和RNFL,结合前面提到PEDF的一些生理功能,这种现象提示我们,PEDF表达的增强可能是包括RGCs在内的视网膜细胞高眼压损伤的一种应激反应.PEDF是一类很有潜力的神经营养因子[13],但它对慢性高眼压条件下视神经节细胞的损伤有何作用?这仍然需要进一步的研究.
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第四军医大学: 1唐都医院眼科,陕西 西安 710038,2全军神经科学研究所, 陕西 西安 710033
作者简介:吕炳健(1975),男(汉族),山东省荣成市人.硕士生(导师 严宏). 上一页 [1] [2] |