Fig. 5

Contribution of attached compounds around CRM28 to neuroinflammation and movement disorder after ischemic stroke. Bone marrow-derived macrophages were treated with 10 µg/mL CRM28 or its core 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 = 5). The data were analyzed using Student’s t test (vehicle group vs. CRM28-treated group) and one-way ANOVA [A F(2, 12) = 36.85, p < 0.0001, B F(2, 12) = 5.875, p = 0.0166, C F(2, 12) = 19.19, p = 0.0002] followed by Dunnett’s multiple comparisons test. Multiple comparisons were corrected by Holm’s method. CRM28 or its core particle was suspended in water and was intranasally (i.n.) administered at a dose of 100 µg/mouse once a day for 7 days. Brain slices were prepared and stained with Iba1 and CD68, and then D amoeboid scores and E the CD68-stained area of the cerebral cortex were calculated. The values are presented as the mean ± S.D. (n = 5). The data were analyzed using Student’s t test with Holm’s correction for multiple comparisons. F After 7 days of exposure to CRM28 or its core, 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 = 9 animals in each group). The area under the curve (AUC) from 1 to 7 days was calculated, and the AUC was analyzed using Student’s t test with Holm’s correction for multiple comparisons. The p values of the vehicle versus 100 µg CRM groups and 100 µg CRM versus 100 µg Core groups were 0.0016 and 0.0342, respectively