摘要
目的 探讨电刺激大鼠小脑顶核对视网膜缺血再灌注损伤的保护作用。方法 大鼠随机分为缺血再灌注组、电刺激组和假手术组。观察视网膜形态学改变 ;用NADPH黄递酶组织化学染色法 (NADPH NDP)观察视网膜内诱导型一氧化氮合酶 (iNOS)的表达 ;采用TUNEL法检测视网膜细胞凋亡情况。结果 (1)缺血再灌注组的内视网膜层 (包括内核层、内丛状层、节细胞 )、神经纤维层和内界膜厚度增加 ,尤其是内丛状层厚度明显高于假手术组 (t=3 6 80 ,P <0 0 1) ;电刺激组的内视网膜厚度与假手术组相比 ,差异无显著意义 (t=1 0 6 4 ,P >0 0 5 ) ;(2 )光镜观察可见缺血再灌注组有明显的细胞核染色质致密浓缩、核碎裂等改变 ,电刺激组仅见少量核浓缩及碎裂 ;(3)电刺激组的iNOS阳性的神经节细胞数明显低于缺血再灌注组 ,其差异有显著意义 (t=3 32 6 ,P <0 0 1) ;(4)电刺激组大鼠发生凋亡的视网膜细胞数明显低于缺血再灌注组 ,其差异有显著意义 (t=4 0 38,P <0 0 1)。结论 电刺激大鼠小脑顶核对缺血再灌注所导致的视网膜组织损伤具有保护作用。
Objective To study the protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia-reperfusion-injury of rat retina. Methods Rats were divided randomly into group of ischemia-reperfusion, group of electrical-stimulation-treated and group of sham-operated. The duration ischemia was 1 hour except sham-operated. In treated group, harvests of retinas followed electrical stimulation of cerebellar fastigial nucleus for 60 min after reperfusion for 6 hours;in reperfusion group, retinas were harvested only after 6 hours reperfusion. Retinal ischemia was produced in rats by ligating vessels and the optic nerve for 1 hour. Expression of inducible nitric oxide synthase (iNOS) in retina was measured by NADPH-NDP histochemistry;Apoptosis was measured by Tdt-dUTP terminal nick-end labeling (TUNEL) method . Morphology change was observed with the help of HPIAS-1000 auto-medical-imagined computer analyzer. Results (1) The thickness of inner retinal (including outer plexiform layer,inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrance) and the inner plexiform layer were increased significantly in ischemia-reperfusion group than those in treated group. (2) The morphological changes of the scattered and condensed nucleus were observed more slightly under light microscopy in treated group than those in ischemia-reperfusion group. (3) Expression of inducible nitric oxide synthase (iNOS) in retinal ganglion cell in treated group is more significant than in ischemia-reperfusion group. (4) The amount of apoptosis cells in retina in treated group is significantly less than thatin ischemia-reperfusion group. Conclusions (1) The results indicated that ischemia-reperfusion injury can induce retinal apoptosis. Retinal apoptosis can be inhibited by electrical stimulation cerebellar fastigial nucleus. (2) iNOS maybe involved in the mechanism of apoptosis. (3) Cerebellar fastigial nucleus electrical stimulation can protect ischemia-reperfused retina.
出处
《中华眼科杂志》
CAS
CSCD
北大核心
2004年第6期400-403,共4页
Chinese Journal of Ophthalmology
