Fig. 7

Increased expression of anti-inflammatory markers in the cortex of NOX2^−/− TBI mice is associated with enhanced IL-10/STAT3 signaling. (a) Protein expression of phosphorylated STAT3 and phosphorylated STAT6 was assessed by western immunoblotting in the ipsilateral cortex of WT and NOX2^−/− sham and TBI mice at 72 h post-injury. (b) pSTAT3 expression was significantly increased in WT and NOX2^−/− TBI mice (^*** P < 0.001, vs. sham; ANOVA). pSTAT3 expression was significantly increased in the cortex of NOX2^−/− TBI mice when compared to WT TBI mice (⁺ P < 0.05, WT TBI vs. NOX2^−/− TBI; ANOVA). (c) TBI significantly increased pSTAT6 expression in the cortex of WT and NOX2^−/− mice (^*** P < 0.001, vs. sham; ANOVA); there was no genotype-related differences in pSTAT6 expression following TBI. (d-i) TBI significantly increased IL-4Rα (d), SOCS3 (e), TGFβ (f), SHIP1 (g), Arg1 (h), and YM1 (i) mRNA expression in the ipsilateral cortex of WT and NOX2^−/−mice at 72 h post-injury (^*** P < 0.001, vs. sham; ANOVA). The expression of each anti-inflammatory marker was significantly increased in NOX2^−/− TBI mice when compared to WT TBI mice (⁺ P < 0.05, ⁺⁺ P < 0.01, WT TBI vs. NOX2^−/− TBI; ANOVA; d-i). All data are expressed as means (±SEM; n = 5)