Fig. 6

Significant role of PAHs included in CRM28 in neuroinflammation and movement disorder after ischemic stroke. Bone marrow-derived macrophages prepared from wild-type and AhR KO mice were treated with 10 µg/mL CRM28 for 6 h, and then mRNA expression of A CYP1A1, B TNFα and C COX-2 was measured by real-time PCR. The values are presented as the mean ± S.D. (n = 6). The data were analyzed using two-way ANOVA [CYP1A1, F(1, 20) = 84.99, p < 0.0001; TNFα, F(1, 20) = 18.55, p = 0.0003; COX-2, F(1, 20) = 24.23, p < 0.0001] with Tukey's corrected multiple comparison tests. CRM28 was suspended in water and intranasally (i.n.) administered at a dose of 100 µg/mouse once a day for 7 days, followed by staining of the cortex region with Iba1 and CD68. D Representative stained pictures of the cerebral cortex. E Amoeboid scores. F The CD68-stained area of the cerebral cortex. The values are presented as the mean ± S.D. (n = 5). The data were analyzed using two-way ANOVA [E: F(1, 16) = 6.251, p = 0.0237; F: F(1, 16) = 8.507, p = 0.0101] with Tukey's corrected multiple comparison tests. G. Coordinated movement was measured by a rotarod test before (day 0) and 1, 3, 5 and 7 days after photothrombosis induction. The reported values are the mean ± S.D. (n = 6 animals in each group). The area under the curve (AUC) from 1 to 7 days was calculated, and the AUC was analyzed using two-way ANOVA [F(1, 20) = 25.97, p < 0.0001] with Tukey's corrected multiple comparison tests. The p values of the wild-vehicle versus wild-CRM groups, AhR KO-vehicle versus AhR KO-CRM groups, and wild-CRM versus AhR KO-CRM groups were < 0.0001, 0.9943 and < 0.0001, respectively