Park Shin Hae, Kim Jie Hyun, Kim Yoon Hee, Park Chan Kee
Department of Ophthalmology, College of Medicine, The Catholic University of Korea, Socho-Gu, Seoul, Republic of Korea.
Vision Res. 2007 Sep;47(21):2732-40. doi: 10.1016/j.visres.2007.07.011. Epub 2007 Sep 6.
We investigated the expression of neuronal nitric oxide synthase (nNOS) in a rat retina model of chronic glaucoma, which was produced by electrocauterization of the episcleral vessels. Western-blot analysis showed that nNOS expression was significantly increased in cauterized retinas. nNOS immunoreactivity was observed in the cells of both the inner nuclear layer and the ganglion cell layer. Double labeling of retinal ganglion cells (RGCs) revealed that RGCs in the retina of cauterized rat was nNOS-immunopositive. Systemic administration of L-NAME (N(G)-nitro-L-arginine-methyl-ester), a non-specific NOS inhibitor, reduced RGC loss in cauterized rat retina, but there was no statistical significance (P =.06). These results suggest that the cytotoxicity of excessive NO plays a role in selective RGC loss in glaucoma.
我们研究了慢性青光眼大鼠视网膜模型中神经元型一氧化氮合酶（nNOS）的表达，该模型通过电烙巩膜血管产生。蛋白质免疫印迹分析表明，电烙视网膜中nNOS表达显著增加。在内核层和神经节细胞层的细胞中均观察到nNOS免疫反应性。视网膜神经节细胞（RGCs）的双重标记显示，电烙大鼠视网膜中的RGCs为nNOS免疫阳性。非特异性一氧化氮合酶抑制剂L-NAME（N(G)-硝基-L-精氨酸甲酯）的全身给药减少了电烙大鼠视网膜中的RGC损失，但无统计学意义（P = 0.06）。这些结果表明，过量一氧化氮的细胞毒性在青光眼选择性RGC损失中起作用。
