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首页> 外文期刊>Translational Stroke Research >Augmentation of Normal and Glutamate-Impaired Neuronal Respiratory Capacity by Exogenous Alternative Biofuels
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Augmentation of Normal and Glutamate-Impaired Neuronal Respiratory Capacity by Exogenous Alternative Biofuels

机译：外源性替代生物燃料增强正常和谷氨酸受损的神经元呼吸能力

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摘要

Mitochondrial respiratory capacity is critical for responding to changes in neuronal energy demand. One approach toward neuroprotection is the administration of alternative energy substrates (“biofuels”) to overcome brain injury-induced inhibition of glucose-based aerobic energy metabolism. This study tested the hypothesis that exogenous pyruvate, lactate, β-hydroxybutyrate, and acetyl-l-carnitine each increase neuronal respiratory capacity in vitro either in the absence of or following transient excitotoxic glutamate receptor stimulation. Compared to the presence of 5 mM glucose alone, the addition of pyruvate, lactate, or β-hydroxybutyrate (1.0–10.0 mM) to either day in vitro (DIV) 14 or 7 rat cortical neurons resulted in significant, dose-dependent stimulation of respiratory capacity, measured by cell respirometry as the maximal O2 consumption rate in the presence of the respiratory uncoupler carbonyl cyanide-p-trifluoromethoxyphenylhydrazone. A 30-min exposure to 100 μM glutamate impaired respiratory capacity for DIV 14, but not DIV 7, neurons. Glutamate reduced the respiratory capacity for DIV 14 neurons with glucose alone by 25 % and also reduced respiratory capacity with glucose plus pyruvate, lactate, or β-hydroxybutyrate. However, respiratory capacity in glutamate-exposed neurons following pyruvate or β-hydroxybutyrate addition was still, at least, as high as that obtained with glucose alone in the absence of glutamate exposure. These results support the interpretation that previously observed neuroprotection by exogenous pyruvate, lactate, or β-hydroxybutyrate is at least partially mediated by their preservation of neuronal respiratory capacity.
机译：线粒体呼吸能力对于响应神经元能量需求的变化至关重要。一种神经保护方法是施用替代性能量底物（“生物燃料”），以克服脑损伤引起的对基于葡萄糖的有氧能量代谢的抑制作用。这项研究检验了以下假设：外源性丙酮酸，乳酸盐，β-羟基丁酸酯和乙酰基-1-肉碱在无瞬态兴奋性毒性谷氨酸受体刺激的情况下或在体外均能增加神经元呼吸能力。与仅5mM葡萄糖存在相比，在体外（DIV）14或7个大鼠皮层神经元中添加丙酮酸，乳酸盐或β-羟基丁酸酯（1.0-10.0mM）可以显着剂量依赖地刺激呼吸能力，通过细胞呼吸测定法在存在呼吸解偶联剂羰基氰化物-对-三氟甲氧基苯基hydr的条件下，作为最大氧气消耗率进行测量。暴露于100μM谷氨酸中30分钟会损害DIV 14（而非DIV 7）神经元的呼吸能力。谷氨酸盐单独使葡萄糖对DIV 14神经元的呼吸能力降低了25％，并且对葡萄糖加上丙酮酸，乳酸或β-羟基丁酸酯的呼吸能力也降低了。然而，添加丙酮酸或β-羟基丁酸酯后，暴露于谷氨酸的神经元的呼吸能力仍然至少与不暴露谷氨酸时单独使用葡萄糖所获得的呼吸能力一样高。这些结果支持以下解释：先前观察到的外源性丙酮酸，乳酸盐或β-羟基丁酸酯的神经保护作用至少部分是由它们对神经元呼吸能力的保存介导的。

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  • 来源
    《Translational Stroke Research》 |2013年第6期|643-651|共9页
  • 作者

    Melissa D. Laird; Pascaline Clerc; Brian M. Polster; Gary Fiskum;

  • 作者单位

    Department of Anesthesiology and the Shock Trauma and Anesthesiology Research Center School of Medicine University of Maryland">(1);

    Department of Anesthesiology and the Shock Trauma and Anesthesiology Research Center School of Medicine University of Maryland">(1);

    Department of Anesthesiology and the Shock Trauma and Anesthesiology Research Center School of Medicine University of Maryland">(1);

    Department of Anesthesiology and the Shock Trauma and Anesthesiology Research Center School of Medicine University of Maryland">(1);

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  • 关键词

    Excitotoxicity; Energy metabolism; Pyruvate; Lactate; β-Hydroxybutyrate; Acetyl-l-carnitine; Mitochondria;

    机译：兴奋毒性能量代谢;丙酮酸盐;乳酸β-羟基丁酸酯;乙酰基肉碱线粒体;

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