scholarly journals Reduced brain edema after traumatic brain injury in mice deficient in P-selectin and intercellular adhesion molecule-1

2000 ◽  
Vol 67 (2) ◽  
pp. 160-168 ◽  
Author(s):  
Michael J. Whalen ◽  
Timothy M. Carlos ◽  
C. Edward Dixon ◽  
Paul Robichaud ◽  
Robert S. B. Clark ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

scholarly journals Disruption of Nrf2 Enhances Upregulation of Nuclear Factor-κB Activity, Proinflammatory Cytokines, and Intercellular Adhesion Molecule-1 in the Brain after Traumatic Brain Injury

2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Jin ◽  
Handong Wang ◽  
Wei Yan ◽  
Lizhi Xu ◽  
Xiaoliang Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Adhesion Molecule ◽  
Proinflammatory Cytokine ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Secondary Brain Injury ◽  
Nuclear Factor ◽  
Wild Type ◽  
Intercellular Adhesion Molecule 1

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 (NF-κB). Enzyme-linked immunosorbent assays were performed to quantify the production of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and interleukin-6 (IL-6). Immunohistochemistry staining experiments were performed to detect the expression of intercellular adhesion molecule-1 (ICAM-1). Nrf2 (−/−) mice were shown to have more NF-κB activation, inflammatory cytokines TNF-α, IL-1βand IL-6 production, and ICAM-1 expression in brain after TBI compared with their wild-type Nrf2 (+/+) counterparts. The results suggest that Nrf2 plays an important protective role in limiting the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI.

Intercellular Adhesion Molecule-1 Expression on Glia Following Brain Injury: Participation of Interleukin-1β

1996 ◽  
Vol 13 (12) ◽  
pp. 801-808 ◽  
Author(s):  
MIKINE SHIBAYAMA ◽  
HIROJI KUCHIWAKI ◽  
SUGURU INAO ◽  
KAZUO YOSHIDA ◽  
MASAFUMI ITO
Keyword(s):  
Brain Injury ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Interleukin 1Β ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1
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