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

Figure 2

NF-κB activity in the cortex of sham and injured Nrf2 (+/+) and Nrf2 (−/−) mice. (a) Nuclear proteins of brain samples of Nrf2 (+/+) and Nrf2 (−/−) mice were assayed for NF-κB DNA binding activity by EMSA 24 hours after TBI. (b) Quantification of NF-κB DNA binding activity was performed by densitometric analysis. The figure indicates that cerebral NF-κB activity was significantly increased after TBI and was greater in Nrf2 (−/−) mice than in Nrf2 (+/+) mice. Data represents mean ± SEM (𝑛=5 per group). ^∗∗𝑃<.01 versus sham control of the same genotype. ^##𝑃<.01 versus injured wild-type mice.

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