Influence of Nrf2 genotype on pulmonary NF-κB activity and inflammatory response after traumatic brain injury

W Jin, L Zhu, Q Guan, G Chen… - Annals of Clinical & …, 2008 - Assoc Clin Scientists
W Jin, L Zhu, Q Guan, G Chen, QF Wang, HX Yin, CH Hang, JX Shi, HD Wang
Annals of Clinical & Laboratory Science, 2008Assoc Clin Scientists
Inflammatory response plays an important role in the pathogenesis of acute lung injury (ALI)
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 explored the influence of Nrf2 genotype on the production of cytokines and on
activation of transcription factors in a murine TBI model. Wild-type Nrf2 (+/+) and Nrf2 (−/−)
deficient mice were subjected to a moderately severe weight-drop impact-acceleration head …
Inflammatory response plays an important role in the pathogenesis of acute lung injury (ALI) 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 explored the influence of Nrf2 genotype on the production of cytokines and on activation of transcription factors in a murine TBI model. Wild-type Nrf2 (+/+) and Nrf2 (−/−) deficient mice were subjected to a moderately severe weight-drop impact-acceleration head injury. Lung wet/dry weight ratio, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and nuclear factor kapp−aB (NF-κB) were investigated at 24 hr after TBI. Nrf2 (−/−) mice were shown to have a greater increase in the lung wet/dry weight ratio compared to their wild-type Nrf2 (+/+) counterparts after TBI. This exacerbation of lung injury in Nrf2 (−/−) mice was associated with increased levels of TNF-α, IL-1β, IL-6, ICAM-1, and their mediator, NF-κB. The results suggest that Nrf2 plays an important protective role in attenuating the pulmonary inflammatory response and NF-κB activation after TBI.
Assoc Clin Scientists