Figure 5
CX3CR1 deficiency attenuates reactive oxygen species generation in brain after middle cerebral artery occlusion. (A) Reactive oxygen species (ROS) were evaluated by Xenogen IVIS200 imager in wild-type (WT) and CX3CR1-/- mice in vivo. (B) Quantification of ROS. No difference in ROS levels were observed between the two groups 24 hours after MCAO. ROS level decreased in CX3CR1-/- mice 72 hours after MCAO compared to 24 hours (P < 0.0001 for genotype and time point, P = 0.0036 for interaction by two-way analysis of variance; **P < 0.01 by Bonferroni post-hoc tests) and is significantly less in CX3CR1-/- mice relative to WT mice (*P < 0.05 by Bonferroni post-hoc tests). n = 6 per group. p/s/cm2/sr, photons per second per centimeter squared per steradian. (C) Immunohistochemistry for 4-hydroxy-2-nonenal (4-HNE) and 8-hydroxy-2-deoxyguanosine (8-OHdG) in the ischemic lesion 24 and 72 hours after MCAO. (D) Reduction of the number of stained cells in the CX3CR1-/- mice compared with WT mice. P < 0.0001 for genotype, P = 0.0003 for oxidative marker, and P = 0.9827 for interaction by two-way analysis of variance. **P < 0.01 by Bonferroni post-hoc tests. n = 5 per group scale bars: 50 μm.