Traumatic brain injury (TBI) is one of the important reason of morbidity and mortality. While the primary injury due to mechanical impact is unavoidable, the secondary injury which is formed as a result of primary injury and thought to occur due to neuroinflammation in the forefront can be prevented and by this way mortality and morbidity can be reduced. High mobility group box-1 (HMGB1) is a protein that triggers the neuroinflammatory process by being released from the nucleus of necrotic tissues after primary injury. The aim of this study is to investigate the effects of HMGB1 on its receptors TLR4 and RAGE, cerebral edema, blood-brain barrier, oxidative stress and apoptosis causing secondary damage in an experimental traumatic brain injury model. Weighing between 280-320 g, 10 to 12 weeks-old, a total of 30 adult male Sprague-Dawley rats were used for the experiments. The rats were randomly assigned to 3 groups: 1) Control, 2) TBI and 3) TBI + ethyl pyruvate group (n = 10 per group). Right parietal cortical contusion was made by using a weight-dropping TBI method. Brain samples were harvested from pericontusional area at 24 h after TBI. HMGB1, TLR4, RAGE, occludin, claudin-5, ZO-1 levels are investigated by western blot analyses and immunohistochemistry examinations. HMGB-1, TLR4 and RAGE expressions increased after TBI. Major tight junction proteins in the blood-brain barrier: occludin, claudin-5 and ZO-1 expressions decreased after TBI. Brain edema increased after TBI. Also, proapoptotic bax and active caspase 3 expressions increased, antiapoptotic bcl-2 levels decreased after TBI. Total oxidant status and oxidative stress increased, total antioxidant status decreased after TBI. HMGB-1 protein plays a key role in the pathophysiology of traumatic brain injury.

中文翻译：

---

在实验性脑损伤模型中，高迁移率的box-1蛋白对脑水肿，血脑屏障，氧化应激和细胞凋亡的影响。

颅脑外伤（TBI）是发病率和死亡率的重要原因之一。尽管由于机械冲击而引起的原发性损伤是不可避免的，但可以预防由于原发性损伤而形成的，被认为是由于最前部的神经发炎而引起的继发性损伤，从而可以降低死亡率和发病率。高迁移率族box-1（HMGB1）是一种蛋白质，可在原发性损伤后从坏死组织的核中释放，从而触发神经炎症过程。这项研究的目的是在实验性脑外伤模型中研究HMGB1对其受体TLR4和RAGE，脑水肿，血脑屏障，氧化应激和凋亡的影响，从而引起继发性损伤。体重在280-320克之间，年龄在10到12周之间，总共使用30只成年雄性Sprague-Dawley大鼠进行实验。将大鼠随机分为3组：1）对照组，2）TBI和3）TBI +丙酮酸乙酯组（每组n ＝ 10）。右顶壁皮质挫伤采用重量减轻TBI法。TBI后24小时从腹膜周围区域收集脑样本。HMGB1，TLR4，RAGE，occludin，claudin-5，ZO-1水平通过蛋白质印迹分析和免疫组织化学检查进行了研究。TBI后HMGB-1，TLR4和RAGE表达增加。TBI后血脑屏障中的主要紧密连接蛋白：occludin，claudin-5和ZO-1表达下降。TBI后脑水肿增加。此外，TBI后促凋亡的bax和活性caspase 3表达增加，抗凋亡的bcl-2水平降低。总氧化剂状态和氧化应激增加，TBI后总抗氧化剂状态下降。HMGB-1蛋白在颅脑外伤的病理生理中起着关键作用。