Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas 77225, USA.
J Neurotrauma. 2013 May 1;30(9):727-40. doi: 10.1089/neu.2012.2650. Epub 2013 May 6.
Mild traumatic brain injury (mTBI), particularly mild "blast type" injuries resulting from improvised exploding devices and many sport-caused injuries to the brain, result in long-term impairment of cognition and behavior. Our central hypothesis is that there are inflammatory consequences to mTBI that persist over time and, in part, are responsible for resultant pathogenesis and clinical outcomes. We used an adaptation (1 atmosphere pressure) of a well-characterized moderate-to-severe brain lateral fluid percussion (LFP) brain injury rat model. Our mild LFP injury resulted in acute increases in interleukin-1α/β and tumor necrosis factor alpha levels, macrophage/microglial and astrocytic activation, evidence of heightened cellular stress, and blood-brain barrier (BBB) dysfunction that were evident as early as 3-6 h postinjury. Both glial activation and BBB dysfunction persisted for 18 days postinjury.
轻度创伤性脑损伤（mTBI），特别是由简易爆炸装置引起的轻度“爆炸型”损伤和许多运动引起的脑损伤，会导致长期的认知和行为障碍。我们的中心假设是，mTBI 存在炎症后果，这些后果会随着时间的推移而持续存在，并且部分原因是导致发病机制和临床结果的原因。我们使用了一种经过很好表征的中度至重度脑侧向液压冲击（LFP）脑损伤大鼠模型的改编版（1 个大气压）。我们的轻度 LFP 损伤导致白细胞介素-1α/β 和肿瘤坏死因子-α 水平的急性增加，巨噬细胞/小胶质细胞和星形胶质细胞的激活，细胞应激的证据以及血脑屏障（BBB）功能障碍，这些损伤早在受伤后 3-6 小时就很明显。胶质细胞激活和 BBB 功能障碍在受伤后 18 天持续存在。
