Crupi Rosalia, Cordaro Marika, Cuzzocrea Salvatore, Impellizzeri Daniela
Department of Veterinary Science, University of Messina, 98168 Messina, Italy.
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Via Consolare Valeria 1, 98100 Messina, Italy.
Antioxidants (Basel). 2020 Apr 2;9(4):297. doi: 10.3390/antiox9040297.
TBI (traumatic brain injury) is a major cause of death among youth in industrialized societies. Brain damage following traumatic injury is a result of direct and indirect mechanisms; indirect or secondary injury involves the initiation of an acute inflammatory response, including the breakdown of the blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors. TBI can cause changes in molecular signaling and cellular functions and structures, in addition to tissue damage, such as hemorrhage, diffuse axonal damages, and contusions. TBI typically disturbs brain functions such as executive actions, cognitive grade, attention, memory data processing, and language abilities. Animal models have been developed to reproduce the different features of human TBI, better understand its pathophysiology, and discover potential new treatments. For many years, the first approach to manage TBI has been treatment of the injured tissue with interventions designed to reduce the complex secondary-injury cascade. Several studies in the literature have stressed the importance of more closely examining injuries, including endothelial, microglia, astroglia, oligodendroglia, and precursor cells. Significant effort has been invested in developing neuroprotective agents. The aim of this work is to review TBI pathophysiology and existing and potential new therapeutic strategies in the management of inflammatory events and behavioral deficits associated with TBI.
创伤性脑损伤（TBI）是工业化社会中青年死亡的主要原因。创伤性损伤后的脑损伤是直接和间接机制共同作用的结果；间接或继发性损伤涉及急性炎症反应的启动，包括血脑屏障（BBB）的破坏、脑水肿、外周血细胞浸润、常驻免疫活性细胞的激活，以及多种免疫介质如白细胞介素和趋化因子的释放。除了组织损伤，如出血、弥漫性轴索损伤和挫伤外，TBI还可导致分子信号传导以及细胞功能和结构的改变。TBI通常会扰乱大脑功能，如执行功能、认知水平、注意力、记忆数据处理和语言能力。已经开发出动物模型来重现人类TBI的不同特征，以便更好地理解其病理生理学，并发现潜在的新治疗方法。多年来，治疗TBI的首要方法一直是通过旨在减少复杂的继发性损伤级联反应的干预措施来治疗受损组织。文献中的几项研究强调了更密切检查损伤的重要性，包括内皮细胞、小胶质细胞、星形胶质细胞、少突胶质细胞和前体细胞。在开发神经保护剂方面已经投入了大量精力。这项工作的目的是综述TBI的病理生理学以及在治疗与TBI相关的炎症事件和行为缺陷方面现有的和潜在的新治疗策略。
