Low level primary blast injury in rodent brain.
Low level primary blast injury in rodent brain.
复制标题
DOI：
10.3389/fneur.2011.00019
复制
发表时间：
2011
影响因子：
3.4
通讯作者：
Lu J
中科院分区：
文献类型：
--
作者：
Pun PB;Kan EM;Salim A;Li Z;Ng KC;Moochhala SM;Ling EA;Tan MH;Lu J
近年来，爆炸袭击和由此造成的创伤性脑损伤的发生率一直在上升。原发性冲击波是冲击波致脑损伤的机制之一。本研究的目的是研究在空旷场地环境中暴露于48.9 kPa（7.1 psi）或77.3 kPa（11.3 psi）的单次亚致死爆炸超压（BOP）对啮齿动物的影响。收集这些大鼠的脑组织用于微阵列和组织病理学分析。大脑的大体组织病理学显示，在爆炸后第1天，大脑皮质中的皮质神经元“变暗”和萎缩，血管变窄，在爆炸后第4天和第7天有恢复的迹象。TUNEL阳性细胞主要分布于爆炸后第1天的脑白色物质中，脑组织的双标记显示，这些DNA损伤的细胞是少突胶质细胞和星形胶质细胞，但由于caspase-3免疫阳性率低，主要不凋亡。白色物质中淀粉样前体蛋白免疫反应细胞也增加，这表明急性轴突损伤。与此相反，Iba-1染色的巨噬细胞或小胶质细胞是没有什么不同，从控制后爆炸。爆炸暴露改变了大脑中超过5786个基因的表达，主要发生在爆炸后第1天和第4天。这些基因被缩小到10个重叠的基因后，时间进程的评估和功能分析。这些基因指向爆炸后第4天和第7天的修复迹象。我们的研究结果表明，研究中的BOP水平导致大脑轻度细胞损伤，表现为急性神经元、脑血管和白色物质扰动，显示出消退迹象。目前还不清楚这些扰动是否存在于较温和的水平或完全正常化，需要更多的调查。基因表达的特异性变化可能被进一步评估，以了解冲击波诱导的神经创伤的机制。
The incidence of blast attacks and resulting traumatic brain injuries has been on the rise in recent years. Primary blast is one of the mechanisms in which the blast wave can cause injury to the brain. The aim of this study was to investigate the effects of a single sub-lethal blast over pressure (BOP) exposure of either 48.9 kPa (7.1 psi) or 77.3 kPa (11.3 psi) to rodents in an open-field setting. Brain tissue from these rats was harvested for microarray and histopathological analyses. Gross histopathology of the brains showed that cortical neurons were “darkened” and shrunken with narrowed vasculature in the cerebral cortex day 1 after blast with signs of recovery at day 4 and day 7 after blast. TUNEL-positive cells were predominant in the white matter of the brain at day 1 after blast and double-labeling of brain tissue showed that these DNA-damaged cells were both oligodendrocytes and astrocytes but were mainly not apoptotic due to the low caspase-3 immunopositivity. There was also an increase in amyloid precursor protein immunoreactive cells in the white matter which suggests acute axonal damage. In contrast, Iba-1 staining for macrophages or microglia was not different from control post-blast. Blast exposure altered the expression of over 5786 genes in the brain which occurred mostly at day 1 and day 4 post-blast. These genes were narrowed down to 10 overlapping genes after time-course evaluation and functional analyses. These genes pointed toward signs of repair at day 4 and day 7 post-blast. Our findings suggest that the BOP levels in the study resulted in mild cellular injury to the brain as evidenced by acute neuronal, cerebrovascular, and white matter perturbations that showed signs of resolution. It is unclear whether these perturbations exist at a milder level or normalize completely and will need more investigation. Specific changes in gene expression may be further evaluated to understand the mechanism of blast-induced neurotrauma.