disruption of nrf2 enhances the upregulation of nuclear factor-kappab activity, tumor necrosis factor- , and matrix metalloproteinase-9 after spinal cord injury in mice中断nrf2核factor-kappab活动,增强了upregulation肿瘤坏死因子和矩阵metalloproteinase-9脊髓损伤后小鼠.pdfVIP

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disruption of nrf2 enhances the upregulation of nuclear factor-kappab activity, tumor necrosis factor- , and matrix metalloproteinase-9 after spinal cord injury in mice中断nrf2核factor-kappab活动,增强了upregulation肿瘤坏死因子和矩阵metalloproteinase-9脊髓损伤后小鼠.pdf

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disruption of nrf2 enhances the upregulation of nuclear factor-kappab activity, tumor necrosis factor- , and matrix metalloproteinase-9 after spinal cord injury in mice中断nrf2核factor-kappab活动,增强了upregulation肿瘤坏死因子和矩阵metalloproteinase-9脊髓损伤后小鼠

Hindawi Publishing Corporation Mediators of Inﬂammation Volume 2010, Article ID 238321, 10 pages doi:10.1155/2010/238321 Research Article Disruption of Nrf2 Enhances the Upregulation of Nuclear Factor-kappaB Activity, Tumor Necrosis Factor-α, and Matrix Metalloproteinase-9 after Spinal Cord Injury in Mice Lei Mao, Handong Wang, Liang Qiao, and Xiaoliang Wang Department of Neurosurgery, School of Medicine, Jinling Hospital, Nanjing University, Nanjing, Jiangsu 210002, China Correspondence should be addressed to Handong Wang, hdwang nj@ Received 20 May 2010; Revised 6 July 2010; Accepted 12 July 2010 Academic Editor: M. Smith Copyright © 2010 Lei Mao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Matrix metalloproteinase-9 (MMP-9) plays an important role in the acute periods of spinal cord injury (SCI), and its expression is related to the inﬂammation which could cause the disruption of the blood-spinal barrier (BBB). 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 upregulating of nuclear factor kappa B (NF-κB) activity, tumor necrosis factor-α (TNF-α), and MMP-9 after SCI. Wild-type Nrf2 (+/+) and Nrf2-deﬁcient (Nrf (−/ −)) mice were subjected to an SCI model induced by the application of vascular clips (force of 10 g) to the dura after a three-level T8-T10 laminectomy. We detected the wet/dry weight ratio of impaired spinal cord tissue, the activation of NF-κB, the mRNA and protein levels of TNF-α and MMP-9, and the enzyme activity of MMP-9. Nrf2 (−/ −) mice were