Blast-induced traumatic brain injury (bTBI) is a leading cause of disability and mortality in soldiers during the conflicts in Iraq and Afghanistan. Although substantial clinical and animal studies have investigated the pathophysiology and treatments of bTBI, few effective therapies have been found, especially for the early rescue in the battlefield. The aim of this study is to evaluate neuroprotective effects of early normobaric hyperoxia (NBO) on bTBI. We established a rat model of bTBI caused by explosion in the cabin. It exhibited typical changes of mild bTBI, like impaired neurological function, brain edema, minor intracranial hemorrhage and neuron necrosis. The rats were divided into 4 groups (n = 12): Sham, Vehicle, hyperbaric oxygen (HBO) and NBO. Neurological function of the rats was assessed by the Neurological Severity Scores (NSS) at 24 h and 72 h after explosion. Serum interleukin-6 (IL-6), neuron specific enolase (NSE) and tau protein were measured at 24 h and 72 h after explosion. Brain water content was measured and Aquaporin-4 (AQP4) immunostaining was performed. Neuronal apoptosis was analyzed by TUNEL staining. NBO demonstrated curative effects on protecting the neurological function. Serum levels of NSE and tau protein were reduced at 24 h and 72 h after explosion. But the levels of IL-6 were not reduced significantly at both time points. Cerebral edema was alleviated. Simultaneously, AQP4 immunostaining of the hippocampus showed remarkably decreased expression after treatment. The number of apoptotic cells in hippocampus was also decreased. Compared with HBO, NBO is simple and convenient, and can be administered in remote areas. It may be a promising therapy for early rescue of bTBI in the battlefield.

爆炸性脑外伤 (bTBI) 是伊拉克和阿富汗冲突期间士兵致残和死亡的主要原因。尽管大量临床和动物研究对 bTBI 的病理生理学和治疗方法进行了调查，但鲜有发现有效的治疗方法，尤其是在战场早期抢救方面。本研究的目的是评估早期常压高氧 (NBO) 对 bTBI 的神经保护作用。我们建立了舱内爆炸引起的bTBI大鼠模型。表现为轻度bTBI的典型改变，如神经功能受损、脑水肿、轻微颅内出血和神经​​元坏死。将大鼠分为 4 组 (n = 12)：Sham、Vehicle、高压氧 (HBO) 和 NBO。在爆炸后 24 小时和 72 小时通过神经严重程度评分 (NSS) 评估大鼠的神经功能。在爆炸后 24 小时和 72 小时测量血清白细胞介素 6 (IL-6)、神经元特异性烯醇化酶 (NSE) 和 tau 蛋白。测量脑含水量并进行 Aquaporin-4 (AQP4) 免疫染色。通过TUNEL染色分析神经元凋亡。NBO 在保护神经功能方面表现出疗效。NSE 和 tau 蛋白的血清水平在爆炸后 24 小时和 72 小时降低。但 IL-6 水平在两个时间点均未显着降低。脑水肿得到缓解。同时，海马AQP4免疫染色显示治疗后表达显着降低。海马中凋亡细胞的数量也减少了。与HBO相比，NBO简单方便，可在偏远地区管理。它可能是战场上早期抢救bTBI的一种有希望的疗法。