The nervous system is one of the first systems to be affected during sepsis. Sepsis not only has a high risk of mortality, but could also lead to cerebral dysfunction and cognitive impairment in long-term survival patients. The receptor for advanced glycation end products (RAGE) can interact with several ligands, and its activation triggers a series of cell signaling events, resulting in the hyperinflammatory condition related to sepsis. Recent studies show that elevated levels of S100B (RAGE ligand) are associated with the pathophysiology of neurodegenerative disorders. They also participate in inflammatory brain diseases and may lead to an increased activation of microglia and astrocytes, leading to neuronal death. This study aimed to determine the effect of S100B inhibition on the neuroinflammatory response in sepsis. Sepsis was induced in Wistar rats by cecal ligation and perforation (CLP). There were three groups: Sham, CLP, and CLP +10 μg/kg of monoclonal antibody (Anti-S100B) administered intracerebroventricularly. The animals were killed 30 days after sepsis following behavioral evaluation by open field, novel object recognition, and splash test. The hippocampus, prefrontal cortex, and amydgala were used for the determination of S100B and RAGE proteins by western blotting and for the evaluation of cytokine levels and verification of the number of microglial cells by immunohistochemistry. On day 30, both the Sham and CLP + anti-S100B groups were capable of recovering the habitual memory in the open field task. Regarding novel object recognition, Sham and CLP + anti-S100B groups increased the recognition index during the test session in comparison to the training session. There was a significant increase in the time of grooming in CLP + anti-S100B in comparison to the CLP group. There was a modulation of cytokine levels and immunohistochemistry showed that the CLP + anti-S100B group had a decrease in the number of microglial cells only in the hippocampus. These results helped to understand the role of S100B protein in the pathophysiology of sepsis-associated encephalopathy and could be helpful to further experimental studies regarding this subject.

神经系统是败血症期间最先受到影响的系统之一。脓毒症不仅具有很高的死亡风险，而且还可能导致长期存活患者的脑功能障碍和认知障碍。晚期糖基化终产物 (RAGE) 受体可以与多种配体相互作用，其激活会触发一系列细胞信号事件，导致与败血症相关的高炎症状态。最近的研究表明，S100B（RAGE 配体）水平升高与神经退行性疾病的病理生理学有关。它们还参与炎症性脑疾病，并可能导致小胶质细胞和星形胶质细胞的活化增加，从而导致神经元死亡。本研究旨在确定 S100B 抑制对脓毒症神经炎症反应的影响。通过盲肠结扎和穿孔 (CLP) 在 Wistar 大鼠中诱导败血症。分为三组：Sham、CLP 和 CLP +10 μg/kg 单克隆抗体（Anti-S100B）脑室内给药。在通过开放场、新物体识别和飞溅试验进行行为评估之后，在败血症后30天处死动物。海马、前额叶皮层和杏仁核用于通过蛋白质印迹法测定 S100B 和 RAGE 蛋白，并通过免疫组织化学评估细胞因子水平和验证小胶质细胞数量。在第 30 天，Sham 组和 CLP + anti-S100B 组都能够恢复野外任务中的习惯性记忆。关于新物体识别，与训练期间相比，假手术组和 CLP + 抗 S100B 组在测试期间提高了识别指数。与 CLP 组相比，CLP + 抗 S100B 的梳理时间显着增加。细胞因子水平发生调节，免疫组织化学显示 CLP + 抗 S100B 组仅在海马体中的小胶质细胞数量减少。这些结果有助于了解 S100B 蛋白在脓毒症相关脑病病理生理学中的作用，并有助于有关该主题的进一步实验研究。细胞因子水平发生调节，免疫组织化学显示 CLP + 抗 S100B 组仅在海马体中的小胶质细胞数量减少。这些结果有助于了解 S100B 蛋白在脓毒症相关脑病病理生理学中的作用，并有助于有关该主题的进一步实验研究。细胞因子水平发生调节，免疫组织化学显示 CLP + 抗 S100B 组仅在海马体中的小胶质细胞数量减少。这些结果有助于了解 S100B 蛋白在脓毒症相关脑病病理生理学中的作用，并有助于有关该主题的进一步实验研究。