一氧化氮合酶在缺血大鼠视网膜中的表达。
Nitric oxide synthase expression in ischemic rat retinas.
作者信息
Kobayashi M, Kuroiwa T, Shimokawa R, Okeda R, Tokoro T
机构信息
Department of Ophthalmology, Faculty of Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
出版信息
Jpn J Ophthalmol. 2000 May-Jun;44(3):235-44. doi: 10.1016/s0021-5155(99)00220-8.
PURPOSE
To investigate the expression of nitric oxide synthase (NOS) in the ischemic retina.
METHODS
Retinal ischemia was induced in rats by bilateral common carotid artery occlusion (BCCAO) for various lengths of time. Using the retina after BCCAO, expression of neuronal NOS (nNOS) and inducible NOS (iNOS) and identification of their positive cells were studied by histological and immunohistochemical examinations.
RESULTS
Histological examinations revealed significant reduction in the thickness of the inner plexiform layer and the outer plexiform layer of the retina. Expression of nNOS was detected in retinal ganglion cells, amacrine cells, and Müller cells after BCCAO. The expression of nNOS and iNOS detected in Müller cells became stronger and persisted long after BCCAO.
CONCLUSIONS
In the ischemic retina, Müller cells and retinal ganglion cells expressed nNOS and iNOS. These phenomena may be involved in the ischemic damage to the retina.
目的
研究一氧化氮合酶（NOS）在缺血视网膜中的表达。
方法
通过双侧颈总动脉闭塞（BCCAO）在大鼠中诱导不同时长的视网膜缺血。利用BCCAO后的视网膜，通过组织学和免疫组织化学检查研究神经元型一氧化氮合酶（nNOS）和诱导型一氧化氮合酶（iNOS）的表达及其阳性细胞的鉴定。
结果
组织学检查显示视网膜内网状层和外网状层厚度显著降低。BCCAO后在视网膜神经节细胞、无长突细胞和Müller细胞中检测到nNOS的表达。在Müller细胞中检测到的nNOS和iNOS的表达在BCCAO后变得更强且持续时间长。
结论
在缺血视网膜中，Müller细胞和视网膜神经节细胞表达nNOS和iNOS。这些现象可能与视网膜的缺血损伤有关。
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