John Curtin School of Medical Research, Australian National University, Acton, Australian Capital Territory, Australia.
Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Kensington, New South Wales, Australia.
J Neurotrauma. 2020 Nov 1;37(21):2244-2260. doi: 10.1089/neu.2020.7066. Epub 2020 Aug 10.
Individuals with spinal cord injury (SCI) often develop debilitating neuropathic pain, which may be driven by neuronal damage and neuroinflammation. We have previously demonstrated that treatment using 670 nm (red) light irradiation alters microglia/macrophage responses and alleviates mechanical hypersensitivity at 7 days post-injury (dpi). Here, we investigated the effect of red light on the development of mechanical hypersensitivity, neuronal markers, and glial response in the subacute stage (days 1-7) following SCI. Wistar rats were subjected to a mild hemi-contusion SCI at vertebra T10 or to sham surgery followed by daily red-light treatment (30 min/day; 670 nm LED; 35 mW/cm) or sham treatment. Mechanical sensitivity of the rat dorsum was assessed from 1 dpi and repeated every second day. Spinal cords were collected at 1, 3, 5, and 7 dpi for analysis of myelination, neurofilament protein NF200 expression, neuronal cell death, reactive astrocytes (glial fibrillary acidic protein [GFAP] cells), interleukin 1 β (IL-1β) expression, and inducible nitric oxide synthase (iNOS) production in IBA1 microglia/macrophages. Red-light treatment significantly reduced the cumulative mechanical sensitivity and the hypersensitivity incidence following SCI. This effect was accompanied by significantly reduced neuronal cell death, reduced astrocyte activation, and reduced iNOS expression in IBA1 cells at the level of the injury. However, myelin and NF200 immunoreactivity and IL-1β expression in GFAP and IBA1 cells were not altered by red-light treatment. Thus, red-light therapy may represent a useful non-pharmacological approach for treating pain during the subacute period after SCI by decreasing neuronal loss and modulating the inflammatory glial response.
脊髓损伤 (SCI) 患者常出现使人虚弱的神经性疼痛，这可能是由神经元损伤和神经炎症引起的。我们之前已经证明，使用 670nm（红色）光照射治疗可改变小胶质细胞/巨噬细胞的反应，并在损伤后 7 天（dpi）缓解机械性超敏反应。在这里，我们研究了红光对 SCI 后亚急性期（第 1-7 天）机械性超敏反应、神经元标志物和神经胶质反应发展的影响。Wistar 大鼠在 T10 椎体处接受轻度半挫伤 SCI，或接受假手术，然后每天接受红光治疗（30 分钟/天；670nm LED；35mW/cm）或假治疗。从 1dpi 开始评估大鼠背部的机械敏感性，并每隔一天重复一次。在 1、3、5 和 7dpi 时收集脊髓，用于分析髓鞘、神经丝蛋白 NF200 表达、神经元细胞死亡、反应性星形胶质细胞（胶质纤维酸性蛋白 [GFAP] 细胞）、白细胞介素 1β（IL-1β）表达和诱导型一氧化氮合酶（iNOS）在 IBA1 小胶质细胞/巨噬细胞中的产生。红光治疗显著降低了 SCI 后的累积机械敏感性和超敏反应发生率。这种效果伴随着损伤水平的神经元细胞死亡减少、星形胶质细胞激活减少和 IBA1 细胞中 iNOS 表达减少。然而，红光治疗并没有改变 GFAP 和 IBA1 细胞中髓鞘和 NF200 免疫反应性和 IL-1β 表达。因此，红光疗法可能通过减少神经元丢失和调节炎症性神经胶质反应，成为 SCI 后亚急性期疼痛治疗的一种有用的非药物治疗方法。
