NADPH氧化酶在缺血性脑卒中诱导的氧化应激中的病理生理学及治疗潜力
Pathophysiology and Therapeutic Potential of NADPH Oxidases in Ischemic Stroke-Induced Oxidative Stress.
作者信息
Duan Jinnan, Gao Shiqi, Tu Sheng, Lenahan Cameron, Shao Anwen, Sheng Jifang
机构信息
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Disease, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
出版信息
Oxid Med Cell Longev. 2021 Mar 9;2021:6631805. doi: 10.1155/2021/6631805. eCollection 2021.
Stroke is a leading cause of death and disability in humans. The excessive production of reactive oxygen species (ROS) is an important contributor to oxidative stress and secondary brain damage after stroke. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, an enzyme complex consisting of membrane subunits and cytoplasmic subunits, regulates neuronal maturation and cerebrovascular homeostasis. However, NADPH oxidase overproduction contributes to neurotoxicity and cerebrovascular disease. NADPH oxidase has been implicated as the principal source of ROS in the brain, and numerous studies have shown that the knockout of NADPH exerts a protective effect in the model of ischemic stroke. In this review, we summarize the mechanism of activation of the NADPH oxidase family members, the pathophysiological effects of NADPH oxidase isoforms in ischemic stroke, and the studies of NADPH oxidase inhibitors to explore potential clinical applications.
中风是人类死亡和残疾的主要原因。活性氧（ROS）的过度产生是中风后氧化应激和继发性脑损伤的重要因素。烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶是一种由膜亚基和细胞质亚基组成的酶复合物，调节神经元成熟和脑血管稳态。然而，NADPH氧化酶的过度产生会导致神经毒性和脑血管疾病。NADPH氧化酶被认为是大脑中ROS的主要来源，许多研究表明，敲除NADPH在缺血性中风模型中具有保护作用。在这篇综述中，我们总结了NADPH氧化酶家族成员的激活机制、NADPH氧化酶亚型在缺血性中风中的病理生理作用以及NADPH氧化酶抑制剂的研究，以探索潜在的临床应用。
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