Angeloni Cristina, Prata Cecilia, Dalla Sega Francesco Vieceli, Piperno Roberto, Hrelia Silvana
Department for Life Quality Studies, Alma Mater Studiorum-University of Bologna, C.so Augusto 237, 47921 Rimini, Italy.
Department of Pharmacy and Biotechnology, Alma Mater Studiorum-University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.
Oxid Med Cell Longev. 2015;2015:370312. doi: 10.1155/2015/370312. Epub 2015 Mar 31.
Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.
创伤性脑损伤（TBI）是全球主要的死亡和残疾原因之一。TBI的特征是创伤直接导致头部受到机械力而产生的原发性损伤，以及随后由于一系列复杂的生化事件导致的继发性损伤，这些生化事件最终导致神经元细胞死亡。氧化应激在导致永久性损伤的延迟有害效应的发生过程中起关键作用。NADPH氧化酶（Nox）是普遍存在的膜多亚基酶，其独特功能是产生活性氧（ROS），已被证明是大脑中ROS的主要来源，并参与多种神经疾病。新出现的证据表明，TBI后Nox上调，提示Nox在该病理过程的发生和发展中起关键作用。在本综述中，我们总结了关于Nox酶在TBI病理生理学中作用的当前证据。
