Figure 5
CKD-506 protected blood–brain barrier integrity in mice with experimental autoimmune encephalitis (EAE) by upregulating occludin expression. Mice were treated with CKD-506 (10, 30, or 100 mg/kg bodyweight) and fingolimod (0.3 mg/kg bodyweight) from day 6 post-EAE induction. The volume of Evans blue dye and the levels of acetylated α-tubulin and occludin in the spinal cord were analyzed 15 days later (a–c). The infiltration of Evans blue dye in the spinal cord of mice with EAE was quantified 1 h after the intravenous injection of the dye (n = 9 per group for the vehicle group; n = 8 per group for the other groups). Additionally, the protein expression levels of acetylated α-tubulin (n = 3 per group) (b) and occludin [n = 8 per group for the non-immunized groups and fingolimod (1 mg/kg) treated group, n = 14 per group for the other groups] (c) in the spinal cord of mice with EAE were evaluated 1 h after the final drug administration on day 21 post-induction. Data are presented as mean ± SD and analyzed using one-way ANOVA, followed by Dunnett’s post-hoc test. #p < 0.05, ##p < 0.01, non-immunized groups versus vehicle group; *p < 0.05, **p < 0.01, and ***p < 0.001, drug-treated group versus vehicle group. N, non-immunized groups; V, vehicle group; Fin, fingolimod (0.3 mg/kg bodyweight)-treated group; CKD, CKD-506 (30 mg/kg bodyweight)-treated group.
