Pharmacologic neuroprotection with an inhibitor of nitric oxide synthase for the treatment of glaucoma
Pharmacologic neuroprotection with an inhibitor of nitric oxide synthase for the treatment of glaucoma
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DOI：
10.1016/j.brainresbull.2003.07.005
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发表时间：
2004-02-15
影响因子：
3.8
通讯作者：
Neufeld, AH
中科院分区：
文献类型：
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作者：
Neufeld, AH
青光眼患者视神经头星形细胞和小胶质细胞中诱导的NOS-2产生的过量一氧化氮可能导致与该疾病相关的视神经病变。建立了慢性中度IOP升高和视网膜神经节细胞缓慢丧失的青光眼大鼠模型，以研究可能具有神经保护作用的药物。在该模型中，氨基胍这种NOS-2抑制剂的药理作用可显著防止视网膜神经节细胞的损失。一种耐受良好的NOS-2药理学抑制剂，可能口服或局部给药，是治疗青光眼的神经保护剂的合理候选。(C) 2003 Elsevier Inc.版权所有。
Excessive nitric oxide, generated by inducible NOS-2 in astrocytes and microglia in the optic nerve head of patients with glaucoma, may contribute to the optic neuropathy associated with the disease. A rat model of glaucoma, in which there is chronic, moderately elevated IOP and slow loss of retinal ganglion cells, has been established to study pharmacological agents that have the potential to be neuroprotective. In this model, the pharmacological use of an inhibitor of NOS-2, aminoguanidine, significantly prevents the loss of retinal ganglion cells. A well-tolerated pharmacological inhibitor of NOS-2, perhaps orally or locally delivered, is a reasonable candidate for a neuroprotective agent for treating glaucoma. (C) 2003 Elsevier Inc. All rights reserved.