Disruption of Nrf2 Enhances Upregulation of Nuclear Factor-B Activity, Proinflammatory Cytokines, and Intercellular Adhesion Molecule-1 in the Brain after Traumatic Brain Injury
Figure 4
Expression of ICAM-1 in the cortex of sham and injured Nrf2 (+/+) and Nrf2 (−/−) mice.
Immunohistochemical staining for ICAM-1 was performed in the cortex tissue sections of Nrf2 (+/+) and Nrf2 (−/−) mice 24 hours
after TBI. (a), (c) Sham-operated Nrf2 (+/+) and Nrf2 (−/−) mice showing few ICAM-1-immunostained cerebral microvessels. (b)
Injured Nrf2 (+/+) mice showing increased number of
ICAM-1 positive vessels. (d) Injured Nrf2 (−/−) mice showing larger increment in the number of ICAM-1 positive vessels compared
with injured Nrf2 (+/+) mice. (e) Quantitative analysis showed that the number of ICAM-1
positive vessels in brain was significantly increased after TBI and was greater
in Nrf2 (−/−) mice than in Nrf2 (+/+) mice. Data
represents mean ± SEM ( per group). ** versus sham control of the same genotype. # versus
injured wild-type mice.
