쥐의 만성 녹내장 모델에서 산화질소 신타아제 동위효소들의 발현

• 영문명: Expression of Nitric Oxide Synthase Isoforms in a Rat Model of Chronic Glaucoma
• 발행기관: 대한안과학회
• 저자명: 김윤희 박찬기,Yoon Hee Kim, M.D., Chan Kee Park, M.D.
• 간행물 정보: 『대한안과학회지』Ophthalmological Society,volume47,number6, 977~985쪽, 전체 9쪽
• 주제분류: 의약학 > 기타의약학
• 파일형태: PDF
• 발행일자: 2006.06.30

영문 초록

Purpose: This study investigated the expression of three isoforms of nitric oxide synthase (NOS): neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) in an experimental rat model of chronic glaucoma. The aim was to research the role of nitric oxide (NO) as a neurotoxic molecule in connection with damage to and the degeneration of retinal ganglion cells in glaucoma. Methods: Retinal tissues were obtained after inducing chronic elevation of intraocular pressure by cauterization of episcleral vessels. We then performed quantification and localization of NOS isoforms through western blot and immuno-fluorescence staining of the tissues. Results: The expression of nNOS and iNOS increased significantly but that of eNOS did not. nNOS expressed in the amacrine and displaced amacrine cell of the normal retinal tissue, as well as in retinal ganglion cells in the experimental group. iNOS that expressed in the microglia of the normal retinal tissue was also expressed in the cell thought to be an astrocyte or Muller cell end-feet in the experimental group. Administration of L-NAME (NG-nitro-L-arginine-methyl-esther), a non-specific NOS inhibitor, tended to reduce retinal ganglion cell loss, but this result was without statistical significance. Conclusions: These results showed that the cytotoxicity of excessive NO took part in retinal ganglion cell loss in glaucoma, and the expression of nNOS in retinal ganglion cells suggests that it may play an important role in the selective death of the retinal ganglion cell.

키워드

Chronic glaucoma, NO, NOS, Retinal ganglion cell loss