Brain and spinal cord interaction: a dietary curcumin derivative counteracts locomotor and cognitive deficits after brain trauma.

Brain and spinal cord interaction: a dietary curcumin derivative counteracts locomotor and cognitive deficits after brain trauma.
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DOI:
10.1177/1545968310397706
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发表时间:
2011-05
影响因子:
4.2
通讯作者:
Gomez-Pinilla F
Gomez-Pinilla F
中科院分区:
医学1区
文献类型:
--
作者:
Wu A;Ying Z;Schubert D;Gomez-Pinilla F

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除了认知功能障碍外,运动缺陷在创伤性脑损伤(TBI)患者中也很普遍;然而,目前尚不清楚脑震荡损伤如何影响脊髓中枢。此外,目前还没有有效的治疗方法可以抵消与TBI相关的广泛病理学。作者研究了TBI对脊髓和海马的破坏性作用的潜在分子基础,以及姜黄素衍生物的神经保护作用,以减少实验性TBI的影响。作者进行了液压冲击损伤(FPI),然后将大鼠暴露于姜黄素衍生物(CNB-001; 500 ppm)的膳食补充剂。咖喱香料姜黄素在神经退行性疾病的动物模型中具有保护能力,姜黄素衍生物具有增强脑吸收和生物活性。结果表明,大鼠的FPI除了降低学习能力外,还降低了运动表现。行为缺陷伴随着对大脑和脊髓中行为可塑性的突触可塑性重要的分子系统的减少。TBI后饮食补充姜黄素衍生物使BDNF水平及其对突触可塑性(CREB,突触蛋白I)和神经元信号传导(CaMKII)的下游效应物以及氧化应激相关分子(SOD,Sir 2)水平正常化。这些研究定义了一种机制,通过这种机制,TBI可以损害与认知处理和运动相关的中心。研究结果还显示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。
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.
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