摘要
目的 已证实色素上皮衍生因子 (pigment epithelium- derived factor,PEDF)对中枢神经细胞有抗凋亡作用。本实验评价其对压力诱发的视网膜缺血再灌注的影响。 方法 经前房灌注维持眼压 110mm Hg(1mm Hg=0 .133k Pa) ,45 min,建立大鼠视网膜缺血再灌注模型。随后立即向玻璃体注射 10 μ1(0 .1μg/ μl) PEDF,分别于 2 d和 7d摘除眼球 ,测量塑料包埋切片的平均视网膜内层厚度 (mean thicknessof inner retinal layer,MTIRL)和视网膜节细胞 (retinal ganglion cells,RGC)计数。 结果 PEDF玻璃体注射 7d后治疗组的 MTIRL和 RGC明显高于对照组 [(118.1± 5 .0 )μm对 (94.9± 3.0 )μm,P<0 .0 5 ;(6 .0±1.0 )个 / 10 0μm对 (4.5± 0 .5 )个 / 10 0μm,P<0 .0 5 ]。 结论 玻璃体内注射
Objective [WT5”BZ]It has been shown that pigment epithelium derived factor (PEDF) is an effective anti apoptosis agent on several kinds of cells of the central nervous system.This study aimed to evaluate the effect of PEDF on pressure induced retinal ischemia in a rat model. Methods Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 45 minutes via an intracameral catheter.Ten microliters (0.1 μg/μl) PEDF was injected into the vitreous of 4 eyes of each group immediately after reperfusion and 4 additional eyes received only normal saline as vehicle controls.The animals were euthanized at 2 or 7 days after reperfusion.The effect of PEDF on retinal degeneration was assessed by measuring the thickness of the inner retinal layers (MTIRL) and counting the retinal ganglion cells (RGC) on plastic embedded retinal sections. [WT5”HZ]Results [WT5”BZ]The MTIRL and the RGC counting in eyes treated with intravitreal PEDF were significantly higher than those in vehicle controls (118.1±5 0) μm vs(94.9±3 0) μm (P<0.05);(6.0±1 0) cells/100 μm vs (4.5±0.5) cells/100 μm (P<0.05) 7 days after reperfusion,respectively. Conclusion Intravitreal administration of PEDF can ameliorate an ischemia reperfusion retinal injury and may be useful to prevent neuronal degeneration in the inner retina.
出处
《中华眼底病杂志》
CAS
CSCD
2001年第2期138-140,共3页
Chinese Journal of Ocular Fundus Diseases
基金
国家自然科学基金!资助项目 (3990 0 0 76)
关键词
色素上皮衍生因子
视网膜血管
神经支配
视网膜缺血
再灌注损伤
大鼠
Pigment epithelium of eye/chemistry
Retinal vessels/innervation
Optic neuropathy,ischemic/drugtherapy
Disease models,animal
Neuroprotective agents