University of California at Los Angeles, Los Angeles, CA, USA.
Neurorehabil Neural Repair. 2011 May;25(4):332-42. doi: 10.1177/1545968310397706. Epub 2011 Feb 22.
In addition to cognitive dysfunction, locomotor deficits are prevalent in traumatic brain injured (TBI) patients; however, it is unclear how a concussive injury can affect spinal cord centers. Moreover, there are no current efficient treatments that can counteract the broad pathology associated with TBI.
The authors have investigated potential molecular basis for the disruptive effects of TBI on spinal cord and hippocampus and the neuroprotection of a curcumin derivative to reduce the effects of experimental TBI.
The authors performed fluid percussion injury (FPI) and then rats were exposed to dietary supplementation of the curcumin derivative (CNB-001; 500 ppm). The curry spice curcumin has protective capacity in animal models of neurodegenerative diseases, and the curcumin derivative has enhanced brain absorption and biological activity.
The results show that FPI in rats, in addition to reducing learning ability, reduced locomotor performance. Behavioral deficits were accompanied by reductions in molecular systems important for synaptic plasticity underlying behavioral plasticity in the brain and spinal cord. The post-TBI dietary supplementation of the curcumin derivative normalized levels of BDNF, and its downstream effectors on synaptic plasticity (CREB, synapsin I) and neuronal signaling (CaMKII), as well as levels of oxidative stress-related molecules (SOD, Sir2).
These studies define a mechanism by which TBI can compromise centers related to cognitive processing and locomotion. The findings also show the influence of the curcumin derivative on synaptic plasticity events in the brain and spinal cord and emphasize the therapeutic potential of this noninvasive dietary intervention for TBI.
除认知功能障碍外，外伤性脑损伤（TBI）患者还普遍存在运动功能障碍；然而， concussion 性损伤如何影响脊髓中枢尚不清楚。此外，目前尚无有效的治疗方法可以对抗与 TBI 相关的广泛病理。
作者研究了 TBI 对脊髓和海马破坏性影响的潜在分子基础，以及姜黄素衍生物对减少实验性 TBI 影响的神经保护作用。
作者进行了液压冲击伤（FPI），然后用姜黄素衍生物（CNB-001；500ppm）对大鼠进行饮食补充。姜黄香料姜黄素在神经退行性疾病的动物模型中具有保护作用，而姜黄素衍生物具有增强大脑吸收和生物活性的作用。
结果表明，大鼠 FPI 除了降低学习能力外，还降低了运动表现。行为缺陷伴随着大脑和脊髓中与行为可塑性相关的突触可塑性的分子系统的减少。TBI 后姜黄素衍生物的饮食补充使 BDNF 及其下游效应物（CREB、突触素 I）和神经元信号（CaMKII）以及与氧化应激相关的分子（SOD、Sir2）的水平正常化。
这些研究定义了 TBI 损害与认知处理和运动相关中心的机制。研究结果还表明了姜黄素衍生物对大脑和脊髓中突触可塑性事件的影响，并强调了这种非侵入性饮食干预对 TBI 的治疗潜力。
