Neuroprotective effects of near-infrared light in an in vivo model of mitochondrial optic neuropathy.
Neuroprotective effects of near-infrared light in an in vivo model of mitochondrial optic neuropathy.
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DOI：
10.1523/jneurosci.3457-08.2008
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发表时间：
2008-12-10
影响因子：
5.3
通讯作者：
Gonzalez-Lima, F.
中科院分区：
文献类型：
--
作者：
Rojas, Julio C.;Lee, Jung;John, Joseph M.;Gonzalez-Lima, F.
关键词：
近红外光（NIL）促进了广泛的生物效应，包括增强能量产生，基因表达和预防细胞死亡。这是第一个报告的在体内的神经保护作用的NIL对视神经病变引起的线粒体复合物I抑制。受试者是接受单次双侧玻璃体内注射鱼藤酮（一种线粒体复合物I抑制剂）或鱼藤酮加三种不同剂量NIL之一的有色大鼠。在行为、结构和神经化学水平上评价治疗效果。鱼藤酮诱导的视觉功能下降，确定在黑暗中适应的照度敏感性阈值，逃避潜伏期和成功的试验率在两个选择的视觉任务的变化，与车辆处理的控制。行为障碍与视网膜和视觉通路代谢活动、视网膜神经纤维层厚度和神经节细胞层细胞密度的降低相关。NIL处理以剂量依赖性方式阻止了这些变化。全脑细胞色素氧化酶和超氧化物歧化酶的活性也增加在近几年治疗的受试者在剂量依赖性的方式，表明在体内经颅效应的近几年。在全脑膜分离株，NIL防止鱼藤酮诱导的细胞呼吸减少。结果表明，NIL治疗可以有效地防止鱼藤酮的神经毒性作用，并可能用于治疗与线粒体功能障碍相关的神经退行性疾病。
Near-infrared light (NIL) promotes a wide range of biological effects including enhancement of energy production, gene expression and prevention of cell death. This is the first report of the in vivo neuroprotective effects of NIL against optic neuropathy induced by mitochondrial complex I inhibition. Subjects were pigmented rats that received single bilateral intravitreal doses of rotenone, a mitochondrial complex I inhibitor, or rotenone plus one of three different doses of NIL. Treatment effects were evaluated at behavioral, structural and neurochemical levels. Rotenone induced a decrease in visual function, as determined by changes in the dark-adapted illuminance sensitivity threshold, escape latency and rate of successful trials in a two-choice visual task, compared to vehicle-treated controls. Behavioral impairment correlated with a decrease in retinal and visual pathway metabolic activity, retinal nerve fiber layer thickness and ganglion cell layer cell density. These changes were prevented by NIL treatments in a dose-dependent manner. Whole-brain cytochrome oxidase and superoxide dismutase activities were also increased in NIL-treated subjects in a dose-dependent manner, suggesting an in vivo transcranial effect of NIL. In whole-brain membrane isolates, NIL prevented the rotenone-induced decrease in cell respiration. The results show that NIL treatment can effectively prevent the neurotoxic effects of rotenone and that it might be used in the treatment of neurodegenerative disorders associated with mitochondrial dysfunction.