Neuroprotection Effect of Ascorbic Acid in Model of Ischemic Retinal Injury.
- Author:
Dong Wook CHOI
1
;
Seong Wook SEO
Author Information
1. Department of Ophthalmology, Gyeongsang National University College of Medicine, Chinju, Korea. stramast@gaechuk.gsnu.ac.kr
- Publication Type:Original Article
- Keywords:
Ascorbic acid;
Ischemic retinal injury;
nNOS;
Neuroprotection
- MeSH:
Animals;
Anterior Chamber;
Ascorbic Acid*;
Ganglion Cysts;
Intraocular Pressure;
Ischemia;
Needles;
Nitric Oxide Synthase Type I;
Rats;
Retina;
Retinaldehyde*
- From:Journal of the Korean Ophthalmological Society
2004;45(8):1348-1355
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: An attempt to establish the neuroprotection effect of ascorbic acid in ischemic retinal injury. METHODS: A rat anterior chamber was cannulated with a 30-gauge infusion needle connected to a container of balanced salt solution (BSS). The container was raised to a height of 3m during 60mins, thereby inducing retina ischemia by high intraocular pressure (HIOP). The effect of ascorbic acid was demonstrated by hematoxylin-eosin (H and E) stain and neuronal nitric oxide synthase (nNOS) immunohistochemical stain. The effect was classified into three HIOP-induced groups: without ascorbic acid treatment, ; ascorbic acid-treated at 24 hr and just before experiment; and ascorbic acid-treated at 24hr, just before experiment and every 24hr after experiment. RESULTS: After retinal ischemia, in the ascorbic acid-treatment groups (Ed- confirm the plural here; from above there are two ascorbic acid-treated groups), the thickness of each retinal layer was preserved more than that in the non-ascorbic acid treated group. There was little difference according to ascorbic acid administration time and period. By nNOS immunohistochemical stain, in the non-ascorbic acid administration group, nNOS immune reactive cells were increased remarkably, in the Inner Nuclear layer (INL) and Ganglion Cell Layer (GCL). In the ascorbic acid-treated groups (Ed-agin confirm), nNOS immune reactive cells were stained in a similar pattern to that of the control group. CONCLUSIONS: The neuroprotection effect of ascorbic acid in ischemic retinal injury was demonstrated, as was the suppression of nNOS expression in the ischemic retina tissue by ascorbic acid administration.
