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饮食疗法促进慢性脊髓损伤的神经保护。

Dietary therapy to promote neuroprotection in chronic spinal cord injury.

机构信息

Department of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-6901, USA.

出版信息

J Neurosurg Spine. 2012 Aug;17(2):134-40. doi: 10.3171/2012.5.SPINE1216. Epub 2012 Jun 26.

Abstract

OBJECT

The pathogenesis of cervical spondylotic myelopathy (CSM) is related to both primary mechanical and secondary biological injury. The authors of this study explored a novel, noninvasive method of promoting neuroprotection in myelopathy by using curcumin to minimize oxidative cellular injury and the capacity of omega-3 fatty acids to support membrane structure and improve neurotransmission.

METHODS

An animal model of CSM was created using a nonresorbable expandable polymer placed in the thoracic epidural space, which induced delayed myelopathy. Animals that underwent placement of the expandable polymer were exposed to either a diet rich in docosahexaenoic acid and curcumin (DHA-Cur) or a standard Western diet (WD). Twenty-seven animals underwent serial gait testing, and spinal cord molecular assessments were performed after the 6-week study period.

RESULTS

At the conclusion of the study period, gait analysis revealed significantly worse function in the WD group than in the DHA-Cur group. Levels of brain-derived neurotrophic factor (BDNF), syntaxin-3, and 4-hydroxynonenal (4-HNE) were measured in the thoracic region affected by compression and lumbar enlargement. Results showed that BDNF levels in the DHA-Cur group were not significantly different from those in the intact animals but were significantly greater than in the WD group. Significantly higher lumbar enlargement syntaxin-3 in the DHA-Cur animals combined with a reduction in lipid peroxidation (4-HNE) indicated a possible healing effect on the plasma membrane.

CONCLUSIONS

Data in this study demonstrated that DHA-Cur can promote spinal cord neuroprotection and neutralize the clinical and biochemical effects of myelopathy.

摘要

目的

颈椎病性脊髓病(CSM)的发病机制与原发性机械损伤和继发性生物损伤有关。本研究作者探索了一种新的、非侵入性的方法,通过使用姜黄素来最小化氧化细胞损伤,以及ω-3 脂肪酸的能力来支持膜结构和改善神经传递,从而促进脊髓病的神经保护。

方法

使用放置在胸硬膜外腔的不可吸收可扩张聚合物创建 CSM 动物模型,该模型可诱导迟发性脊髓病。接受可扩张聚合物放置的动物暴露于富含二十二碳六烯酸和姜黄素(DHA-Cur)的饮食或标准西方饮食(WD)中。27 只动物进行了连续步态测试,并在 6 周研究期后进行了脊髓分子评估。

结果

在研究结束时,步态分析显示 WD 组的功能明显比 DHA-Cur 组差。在受压迫的胸段和腰段扩张处测量脑源性神经营养因子(BDNF)、突触融合蛋白-3 和 4-羟基壬烯醛(4-HNE)的水平。结果表明,DHA-Cur 组的 BDNF 水平与完整动物无显著差异,但明显高于 WD 组。DHA-Cur 动物的腰椎扩张突触融合蛋白-3 明显升高,同时脂质过氧化(4-HNE)减少,表明对质膜可能有修复作用。

结论

本研究数据表明,DHA-Cur 可促进脊髓神经保护,并中和脊髓病的临床和生化影响。

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