Fig. 6.

14,15-EEZE application abolished the neuroprotective effect of hepatic sEH ablation in the CCI mouse model. (A) Representative images of Nissl staining for WT and cKO mice treated with ACSF or 14,15-EEZE. The red outline shows the loss area of injured brain. (B) Quantitative analysis of brain lesion volume (n = 6). (C–E) Behavioral changes in the OFT (C), rotarod performance test (D), and Y-maze test (E) in WT and cKO mice treated with ACSF or 14,15-EEZE (n = 12). (F) The increased mRNA levels of neuroprotective factors in the injured cortex induced by hepatic sEH ablation were blocked by 14,15-EEZE (dashed line indicates the mean levels of each corresponding gene in WT controls treated with ACSF, n = 12). (G) Relative mRNA levels of genes associated with A2 phenotype astrocytes in the injured cortex (dashed line indicates the mean levels of each corresponding gene in WT controls treated with ACSF, n = 12). Statistical significance was determined using two-way ANOVA followed by the Bonferroni’s post-hoc test for B, C, and E–G; or two-way repeated-measures ANOVA followed by the Bonferroni’s post-hoc test for D. Data are presented as the means ± SEM. Asterisks or plus signs indicate significant differences (*P < 0.05, **P < 0.01, ***P < 0.001 vs. ACSF-treated WT mice; ⁺P < 0.05, ⁺⁺P < 0.01, ⁺⁺⁺P < 0.001 vs. ACSF-treated cKO mice).