Induction of monocarboxylate transporter 2 expression and ketone transport following traumatic brain injury in juvenile and adult rats
Induction of monocarboxylate transporter 2 expression and ketone transport following traumatic brain injury in juvenile and adult rats
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DOI：
10.1159/000094170
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发表时间：
2006-01-01
影响因子：
2.9
通讯作者：
Giza, C. C.
中科院分区：
文献类型：
--
作者：
Prins, M. L.;Giza, C. C.
基于最近的工作证明创伤性脑损伤（TBI）后年龄依赖性生酮神经保护，假设早期断奶后动物的神经保护与损伤后酮的诱导脑转运有关。在出生后35天和成年大鼠中，用免疫组织化学方法对假手术或控制性皮质撞击损伤后单羧酸转运体2（MCT 2）的区域变化进行了急性检查。两个年龄组在TBI后同侧脑血管中的MCT 2表达均升高。使用蛋白质印迹法，MCT 2的表达是80-88%，从出生后第35天的大鼠在所有时间点相对于成人分离的微血管。当损伤后可获得酮时，MCT 2表达的增加与年龄相关的脑酮摄取增加在时间上相关。版权所有（c）2006 S. Karger AG，巴塞尔。
Based on recent work demonstrating age-dependent ketogenic neuroprotection after traumatic brain injury (TBI), it was hypothesized that the neuroprotection among early post-weaned animals was related to induced cerebral transport of ketones after injury. Regional changes in monocarboxylate transporter 2 (MCT2) were acutely examined with immunohistochemistry after sham surgery or controlled cortical impact injury among postnatal day 35 and adult rats. Both ages showed elevated MCT2 expression in the ipsilateral cerebral vasculature after TBI. Using Western blotting, MCT2 expression was 80-88% greater in microvessels isolated from postnatal day 35 rats at all time points relative to adults. The increased MCT2 expression was temporally correlated with an age-related increase in cerebral uptake of ketones, when ketones were made available after injury. Copyright (c) 2006 S. Karger AG, Basel.