By observing the dynamic changes of extracellular histones H1, H2A, H4, and NF-κB expression in brain tissues after brain injury in rats, we explore the association among the expression of extracellular histones H1, H2A, H4, and NF-κB following traumatic brain injury (TBI), as well as the effect of different atmospheres absolute hyperbaric oxygen (HBO) intervention on the expression and possible mechanisms. A total of 120 SD rats were randomly divided into 4 groups: Sham-operated (SH), TBI (traumatic brain injury) group, traumatic brain injury and hyperbaric oxygen treatment 1.6ATA (TBI + HBO1) group, and traumatic brain injury and hyperbaric oxygen treatment2.2ATA (TBI + HBO2) group, with 30 rats in each group. The rats in each group were then randomly divided into five smaller time-specific sub-groups: 3 h, 6 h, 12 h, 24 h, and 48 h after surgery. TBI models were established, and the brain tissue around the lesion was taken at different time points. On the one hand,we detected the level of local histones H1, H2A, H4, and NF-κB by RT-PCR and Western Blot. On the other hand, we used immunohistochemical methods to detect the expression of NF-κB, while using the TUNEL method to observe the cell apoptosis in experimental groups after brain injury. Extracellular histones H1, H2A, H4, and NF-κB proteins were highly expressed at 3 h, then with a slight fluctuation, reached to peak at 48 h after the injury. HBO can affect the expression of histones H1, H2A, H4, and NF-κB. The decline of each indicator in the 1.6ATA group was significantly lower than that in the 2.2ATA group, especially within 6 h (P < 0. 05). In addition, NF-κB expression was consistent with the pathological changes of apoptosis in experimental groups. Hyperbaric oxygen therapy with relatively low pressure (1.6ATA) at the early stage can significantly inhibit the expression of extracellular histones H1, H2A, H4, and NF-κB around the lesion, reduce the apoptosis of nerve cells, and thus play an important role in alleviating secondary brain injury.

通过观察大鼠脑损伤后脑组织中细胞外组蛋白 H1、H2A、H4、NF-κB 表达的动态变化，探讨创伤后细胞外组蛋白 H1、H2A、H4、NF-κB 表达的相关性。脑损伤（TBI）以及不同气氛绝对高压氧（HBO）干预对其表达的影响及可能的机制。 120只SD大鼠随机分为4组:假手术组(SH)、TBI(脑外伤)组、脑外伤+高压氧治疗1.6ATA(TBI+HBO1)组、脑外伤+高压氧治疗组。氧治疗2.2ATA(TBI+HBO2)组,每组30只。然后将每组大鼠随机分为五个较小的特定时间亚组：术后3小时、6小时、12小时、24小时和48小时。建立TBI模型，并在不同时间点采集病灶周围脑组织。一方面，通过RT-PCR和Western Blot检测局部组蛋白H1、H2A、H4和NF-κB的水平。另一方面，我们采用免疫组化方法检测NF-κB的表达，同时采用TUNEL法观察实验组脑损伤后细胞凋亡情况。细胞外组蛋白H1、H2A、H4和NF-κB蛋白在损伤后3 h表达量最高，随后略有波动，在损伤后48 h达到峰值。 HBO 可影响组蛋白 H1、H2A、H4 和 NF-κB 的表达。 1.6ATA 组各项指标下降幅度均显着低于 2.2ATA 组，尤其是 6 h 内（ P < 0. 05）。另外，实验组中NF-κB的表达与细胞凋亡的病理变化一致。 早期相对低压（1.6ATA）的高压氧治疗可显着抑制病灶周围细胞外组蛋白H1、H2A、H4、NF-κB的表达，减少神经细胞的凋亡，从而发挥重要作用减轻继发性脑损伤。