As we all know, TNF-α, IL-1β, and IL-6 are regulated by NF-κB and reflect the endogenous activity of NF-κB. It has been revealed that these proinflammatory cytokines are increased after TBI in animals [2, 8]. And our previous study has proved that higher levels of such proinflammatory cytokines were observed in the brain of Nrf2-deficient mice after TBI [5]. But it is still ambiguous about the relationship between these cytokines and Nrf2 in astrocytes after TBI. Here, we tested the levels of TNF-α, IL-1β, and IL-6 in cultured astrocytes at 24 h after scratch injury by RT-PCR and ELISA. It was shown that the mRNA levels of TNF-α, IL-1β, and IL-6 were increased after scratch in both WT and KO astrocytes when compared with their sham counterparts, respectively. Moreover, the mRNA levels of these cytokines in group KO TBI were much higher than those in group WT TBI (1.66 ± 0.085 versus 1.39 ± 0.110 for TNF-α, 1.34 ± 0.064 versus 0.73 ± 0.088 for IL-1β, and 1.28 ± 0.102 versus 0.99 ± 0.073 for IL-6. P < 0.01) (Figures 3(a)–3(d)). The results of ELISA revealed that the protein level of TNF-α was upregulated after scratch injury in WT and KO astrocytes when compared with their sham counterparts. And it was also higher in group KO TBI than in group WT TBI (3.67 ± 0.156 versus 2.31 ± 0.087, P < 0.01) (Figure 4(a)). Similar tendency was observed in protein level of IL-6 and IL-1β. For IL-6, it was 36.07 ± 0.786 for group KO TBI while 25.76 ± 0.536 for group WT TBI (P < 0.01) (Figure 4(b)). For IL-1β, it was 190.75 ± 6.339 for group KO TBI while 154.50 ± 5.348 for group WT TBI (P < 0.01) (Figure 4(c)).