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Annals of Clinical & Laboratory Science 38:221-227 (2008)
© 2008 Association of Clinical Scientists

Influence of Nrf2 Genotype on Pulmonary NF-{kappa}B Activity and Inflammatory Response after Traumatic Brain Injury

Wei Jin1, Lin Zhu1, Qun Guan2, Gang Chen1, Qing Feng Wang1, Hong Xia Yin1, Chun Hua Hang1, Ji Xin Shi1 and Han Dong Wang1
1 Departments of Neurosurgery and 2 Obstetrics & Gynecology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China

Address correspondence to Dr. Han Dong Wang, Department of Neurosurgery, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, P. R. China; tel 86 25 8481 7581; fax 86 25 8481 7581; e-mail hdwang_nj{at}yahoo.com.cn.

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-{alpha} (TNF-{alpha}), interleukin-1β (IL-1β), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and nuclear factor kapp–aB (NF-{kappa}B) 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-{alpha}, IL-1β, IL-6, ICAM-1, and their mediator, NF-{kappa}B. The results suggest that Nrf2 plays an important protective role in attenuating the pulmonary inflammatory response and NF-{kappa}B activation after TBI.

Keywords: traumatic brain injury, lung, Nrf2, NF-{kappa}B, cytokines, pulmonary inflammatory response






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