Metabolic Acetate Therapy for the Treatment of Traumatic Brain Injury
Metabolic Acetate Therapy for the Treatment of Traumatic Brain Injury
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DOI：
10.1089/neu.2009.0994
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发表时间：
2010-01-01
影响因子：
4.2
通讯作者：
Namboodiri, Aryan M. A.
中科院分区：
文献类型：
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作者：
Arun, Peethambaran;Ariyannur, Prasanth S.;Namboodiri, Aryan M. A.
患有创伤性脑损伤（TBI）的患者具有降低的能量代谢标志物，包括N-乙酰天冬氨酸（NAA）和ATP。在神经系统中，NAA衍生的乙酸盐提供髓鞘脂质合成所需的乙酰辅酶A。乙酸盐也可以在线粒体中被氧化，以获得代谢能量。在目前的研究中，使用控制皮质撞击模型TBI大鼠，我们调查的疏水性乙酸酯前体，甘油三乙酸酯（GTA），作为一种方法，提供代谢乙酸受伤的大脑的影响。我们发现，GTA管理显着增加受伤的半球NAA和ATP的水平在受伤后4和6天，也导致在受伤后3天大鼠的运动表现显着改善。
Patients suffering from traumatic brain injury (TBI) have decreased markers of energy metabolism, including N-acetylaspartate (NAA) and ATP. In the nervous system, NAA-derived acetate provides acetyl-CoA required for myelin lipid synthesis. Acetate can also be oxidized in mitochondria for the derivation of metabolic energy. In the current study, using the controlled cortical impact model of TBI in rats, we investigated the effects of the hydrophobic acetate precursor, glyceryltriacetate (GTA), as a method of delivering metabolizable acetate to the injured brain. We found that GTA administration significantly increased the levels of both NAA and ATP in the injured hemisphere 4 and 6 days after injury, and also resulted in significantly improved motor performance in rats 3 days after injury.