Fig. 2

Expression of astrocytic sEH regulated the LPS-induced expression of pro-inflammatory markers. The LPS-induced protein expression levels of pro-inflammatory markers in si-sEH primary astrocytes (n = 9), including iNOS (p < 0.01) and COX-2 (p < 0.05), were significantly increased compared to those in the controls (n = 9), while over-sEH astrocytes (n = 8) showed a reduction in LPS-induced expression levels of iNOS (p < 0.001) and COX-2 (p < 0.001) (a). Similarly, the secretion of LPS-induced TNFα and IL-6 from primary astrocytes derived from sEH^−/− mice (n = 12) was significantly increased (p < 0.001 for both) compared to the LPS-treated controls (n = 10), while the secretion of TNFα and IL-6 from over-sEH astrocytes (n = 4) was reduced (p < 0.05 for both) compared to the LPS-treated controls (n = 4) (b). In si-sEH astrocytes (n = 4), IL-6 secretion was significantly increased (p < 0.001) compared to the LPS-treated controls (n = 4), while TNFα was slightly increased compared to the LPS-treated controls. Changes in the expression level of sEH had no effects on the basal immunity of astrocytes without the challenge of LPS. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA and Bonferroni multiple comparison test. *p < 0.05, **p < 0.01, ***p < 0.001