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神经保护素D1可抑制轴突切断后视网膜神经节细胞的死亡。

Neuroprotectin D1 inhibits retinal ganglion cell death following axotomy.

作者信息

Qin Qiong, Patil Kiran A, Gronert Karsten, Sharma Sansar C

机构信息

Department of Cell Biology and Anatomy and Ophthalmology, New York Medical College, Valhalla, NY 10595, USA.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2008 Dec;79(6):201-7. doi: 10.1016/j.plefa.2008.09.022. Epub 2008 Nov 18.

DOI:10.1016/j.plefa.2008.09.022
PMID:19019647
Abstract

Neuroprotectin D1 (NPD1), a docosahexaenoic acid-derived autacoid, is an endogenous neuroprotective and anti-inflammatory mediator that is generated in the retina and brain. The effects of exogenous NPD1 on retinal ganglion cell (RGC) apoptosis and the role of 12/15-lipoxygenase (Alox15) in retina were evaluated after optic nerve transection (ONT). Treatment with NPD1 was associated with significant protection against RGC death. The percentage of RGC survival in NPD1-treated group was 30% at 2 weeks after ONT as compared with 12% of RGC survival in the ONT group without treatment. Endogenous NPD1 was a predominant lipid autocoid in uninjured and axotomized retinas. Alox15 mRNA expression was upregulated in retinas following ONT suggesting that amplification of 12/15-lipoxygenase (12/15-LOX) may represent a neuroprotective response in the rat retina. The density of RGCs was higher in the normal retina of 12/15-LOX-deficient mice as compared with congenic controls. Hence, the resident NPD1 has a potential role in the physiological and pathophysiological responses of the retina.

摘要

神经保护素D1(NPD1)是一种源自二十二碳六烯酸的自分泌调节物质,是一种内源性神经保护和抗炎介质,在视网膜和大脑中产生。在视神经横断(ONT)后,评估了外源性NPD1对视网膜神经节细胞(RGC)凋亡的影响以及12/15-脂氧合酶(Alox15)在视网膜中的作用。NPD1治疗与对RGC死亡的显著保护相关。ONT后2周,NPD1治疗组RGC存活百分比为30%,而未治疗的ONT组RGC存活百分比为12%。内源性NPD1是未受伤和轴突切断的视网膜中主要的脂质自分泌调节物质。ONT后视网膜中Alox15 mRNA表达上调,提示12/15-脂氧合酶(12/15-LOX)的扩增可能代表大鼠视网膜中的一种神经保护反应。与同基因对照相比,12/15-LOX缺陷小鼠正常视网膜中RGC的密度更高。因此,内源性NPD1在视网膜的生理和病理生理反应中具有潜在作用。

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