Low-level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro.
Low-level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro.
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DOI：
10.1002/jbio.201300125
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发表时间：
2014-08
影响因子：
2.8
通讯作者：
Hamblin, Michael R.
中科院分区：
文献类型：
--
作者：
Huang, Ying-Ying;Nagata, Kazuya;Tedford, Clark E.;Hamblin, Michael R.
关键词：
兴奋性毒性描述了一种致病过程，其中神经元死亡释放大量兴奋性神经递质谷氨酸，然后继续激活邻近神经元上的一组谷氨酸能受体（谷氨酸，N-甲基-D-天冬氨酸（NMDA）和红藻氨酸），打开离子通道，导致钙离子流入，产生线粒体功能障碍和细胞死亡。兴奋性毒性导致中风后的脑损伤、创伤性脑损伤和神经退行性疾病，并且还涉及脊髓损伤。我们测试了810 nm的低水平激光（光）治疗（LLLT）是否可以保护原代培养的小鼠皮层神经元免受谷氨酸、NMDA或红藻氨酸在体外产生的兴奋性毒性。虽然对细胞死亡的预防是适度的，但显著的，LLLT（在25 mW/cm 2下递送3 J/cm 2，持续2分钟）在增加ATP、提高线粒体膜电位、降低细胞内钙浓度、降低氧化应激和减少一氧化氮方面具有非常显著的益处。LLLT在消除兴奋性毒性中的作用可能在解释其在各种中枢神经系统病理中的有益作用方面发挥作用。（（图：5a））810 nm激光对兴奋性毒性皮层神经元细胞内活性氧的影响
Excitotoxicity describes a pathogenic process whereby death of neurons releases large amounts of the excitatory neurotransmitter glutamate, which then proceeds to activate a set of glutamatergic receptors on neighboring neurons (glutamate, N-methyl-D-aspartate (NMDA), and kainate), opening ion channels leading to an influx of calcium ions producing mitochondrial dysfunction and cell death. Excitotoxicity contributes to brain damage after stroke, traumatic brain injury, and neurodegenerative diseases, and is also involved in spinal cord injury. We tested whether low level laser (light) therapy (LLLT) at 810-nm could protect primary murine cultured cortical neurons against excitotoxicity in vitro produced by addition of glutamate, NMDA or kainate. Although the prevention of cell death was modest but significant, LLLT (3 J/cm2 delivered at 25 mW/cm2 over 2 min) gave highly significant benefits in increasing ATP, raising mitochondrial membrane potential, reducing intracellular calcium concentrations, reducing oxidative stress and reducing nitric oxide. The action of LLLT in abrogating excitotoxicity may play a role in explaining its beneficial effects in diverse central nervous system pathologies. ((Figure: 5a)) Effect of 810-nm laser on intracellular reactive oxygen species (ROS) in cortical neurons with excitotoxicity
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