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. Author manuscript; available in PMC: 2015 Sep 10.
Published in final edited form as: Neuroendocrinology. 2014 Sep 10;100(0):129–140. doi: 10.1159/000367849

Fig. 4.

Fig. 4

GCs alter chemokine release post-injury. CA3 tissue was collected at 2, 4, 8, 12, 18, 24, and 48 h post-KA injury. n = 3–6 per group. (A) CCL2 production peaked at 18 h post-KA and was significantly elevated over sham animals in both low GC and high GC groups at 8 h and continued to be elevated in low GC animals from 18 to 24 h. Significance levels * p < 0.05 and ** p < 0.01 established by 2-way ANOVA followed by Holm-Sidak post hoc test. Significant 2-way ANOVA main effect of time post-injury (p < 0.0001). (B) CCL2 production at 8 hours post-injury was significantly higher in low GC animals compared to sham. Significance established by 1-way ANOVA followed by Holm-Sidak post hoc test. Significant 1-way ANOVA main effect (p < 0.05). (C) CINC-1 production peaked at 8 h post-KA and was increased in high GC animals relative to sham. Significance established by 2-way ANOVA followed by Holm-Sidak post hoc test. Significant 2-way ANOVA main effect of time post-injury (p < 0.0001) and significant interaction (p < 0.01). (D) CINC-1 production at 8 hours post-injury was significantly higher in animals given 100% GC pellets compared to those given 30%. Significance established by 1-way ANOVA followed by Holm-Sidak post hoc test. Significant 1-way ANOVA main effect (p < 0.01).