disruption of nrf2 enhances upregulation of nuclear factor- b activity, proinflammatory cytokines, and intercellular adhesion molecule-1 in the brain after traumatic brain injury中断nrf2增强upregulation核因子- b活动,促炎细胞因子和细胞间粘附molecule-1创伤性脑损伤后在大脑中.pdfVIP

Hindawi Publishing Corporation Mediators of Inflammation Volume 2008, Article ID 725174, 7 pages doi:10.1155/2008/725174 Research Article Disruption of Nrf2 Enhances Upregulation of Nuclear Factor-κB Activity, Proinflammatory Cytokines, and Intercellular Adhesion Molecule-1 in the Brain after Traumatic Brain Injury Wei Jin,1 Handong Wang,1 Wei Yan,2 Lizhi Xu,3 Xiaoliang Wang,1 Xiaoning Zhao,3 Xiaohe Yang,3 Gang Chen,1 and Yan Ji4 1 Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, Jiangsu Province, China 2 Department of Neurosurgery, Second Affi liated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, Zhejiang Province, China 3 Department of Medical Genetics, School of Medicine, Nanjing University, Nanjing 210093, Jiangsu Province, China 4 Department of Oral and Maxillofacial Surgery, Affi liated Stomatology Hospital, School of Medicine, Nanjing University, Nanjing 210008, Jiangsu Province, China Correspondence should be addressed to Handong Wang, hdwang jw@ Received 18 August 2008; Accepted 10 November 2008 Recommended by Oreste Gualillo Inflammatory response plays an important role in the pathogenesis of secondary brain injury after traumatic brain injury (TBI). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI. Wild-type Nrf2 (+/+) and Nrf2 (−/ −)-deficient mice were subjected to a moderately severe weight-drop impact head injury. Electrophoretic mobility shift assays (EMSAs) were performed to analyze the activation of nuclear factor kappa B