Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function.
Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function.
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DOI：
10.1186/2051-5960-1-57
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发表时间：
2013-09-06
影响因子：
7.1
通讯作者：
Rogozinska M
中科院分区：
文献类型：
--
作者：
Briones TL;Woods J;Rogozinska M
持续的神经炎症和脑能量代谢的中断在创伤性脑损伤（TBI）中常见。由于大多数TBI干预措施缺乏成功，以及环境丰富（EE）在增强大脑可塑性方面的记录益处，在这里，我们将研究重点放在EE在调节损伤诱导的神经炎症和前额叶皮层和海马能量代谢中断中的应用上。成年雄性Wistar大鼠用于研究，并随机分配接受：轻度TBI（mTBI）使用受控皮质损伤模型或假手术。手术后，将各组大鼠进一步随机分配至EE饲养区或标准实验室饲养区（CON）。恢复4周后，使用非匹配样本和延迟非匹配样本任务进行认知测试。完成行为测试后，测量促炎细胞因子IL-1β和TNF-α以及抗炎细胞因子IL-10的水平。此外，评估AMPK（腺苷一磷酸活化蛋白激酶）、磷酸化AMPK和uMtCK（普遍存在的线粒体肌酸激酶）的水平作为脑能量稳态的量度。我们的研究结果表明，EE：（1）降低mTBI后促炎细胞因子IL-1β和TNF-α的水平，提高抗炎细胞因子IL-10的水平;（2）减轻mTBI诱导的认知障碍;（3）减弱mTBI诱导的pAMPK/AMPK比值和uMtCK水平的下调。我们的数据表明EE调节持续性的潜力：（1）mTBI后观察到的神经炎症反应，和（2）脑能量稳态的持续性紊乱。这可能是通过调节神经炎症的机制，EE住房能够恢复能量代谢的中断和增强mTBI后的功能恢复。
Persistent neuroinflammation and disruptions in brain energy metabolism is commonly seen in traumatic brain injury (TBI). Because of the lack of success of most TBI interventions and the documented benefits of environmental enrichment (EE) in enhancing brain plasticity, here we focused our study on use of EE in regulating injury-induced neuroinflammation and disruptions in energy metabolism in the prefrontal cortex and hippocampus. Adult male Wistar rats were used in the study and randomly assigned to receive either: mild TBI (mTBI) using the controlled cortical injury model or sham surgery. Following surgery, rats from each group were further randomized to either: EE housing or standard laboratory housing (CON). After 4 weeks of recovery, cognitive testing was performed using the non-matching-to-sample and delayed non-matching-to-sample tasks. After completion of behavioral testing, levels of the pro-inflammatory cytokines IL-1β and TNF-α and the anti-inflammatory cytokine IL-10 were measured. In addition, levels of AMPK (adenosine monophosphate-activated protein kinase), phosphorylated AMPK and uMtCK (ubiquitous mitochondrial creatine kinase) were assessed as measures of brain energy homeostasis. Our results showed that EE: (1) decreased the pro-inflammatory cytokines IL-1β and TNF-α and enhanced levels of the anti-inflammatory cytokine IL-10 after mTBI; (2) mitigated mTBI-induced cognitive impairment; and (3) attenuated mTBI-induced downregulation in pAMPK/AMPK ratio and uMtCK levels. Our data demonstrated the potential of EE to modulate the persistent: (1) neuroinflammatory response seen following mTBI, and (2) persistent disturbance in brain energy homeostasis. It is possible that through the mechanism of modulating neuroinflammation, EE housing was able to restore the disruption in energy metabolism and enhanced functional recovery after mTBI.
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影响因子：
2.5
作者：
Briones, T L;Therrien, B;Metzger, B
通讯作者：
Metzger, B
影响因子：
2.7
作者：
Briones, TL;Woods, J;Nguyen, M
通讯作者：
Nguyen, M
影响因子：
4.2
作者：
Cheng, Jeffrey P.;Shaw, Kaitlyn E.;Kline, Anthony E.
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Kline, Anthony E.
影响因子：
4.3
作者：
Boero, J;Qin, W;Khuchua, Z
通讯作者：
Khuchua, Z
影响因子：
4.3
作者：
Kovesdi E;Gyorgy AB;Kwon SK;Wingo DL;Kamnaksh A;Long JB;Kasper CE;Agoston DV
通讯作者：
Agoston DV