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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Recombinant CCL17-dependent CCR4 activation alleviates neuroinflammation and neuronal apoptosis through the PI3K/AKT/Foxo1 signaling pathway after ICH in mice

Fig. 2

To evaluate the role of endogenous CCL17 and CCR4 after ICH. Endogenous CCL17 and CCR4 increased at 72 h after ICH. Anti-CCL17 mAb and C021 abolished the effect of endogenous CCL17 and CCR4 and increased inflammatory markers at 72 h after ICH (a, b). Intranasal administration of rCCL17 (1 h, 3 h, and 6 h) improved neurological function. *p<0.05 vs sham, @p<0.05 vs ICH + control mAb, #p<0.05 vs ICH + Anti-CCL17 mAb, $p<0.05 vs ICH +DMSO, One-way ANOVA, Tukey’s test, n=6/group. c Behavior tests. Left forelimb placement test (c), Corner turn test(c) and Modified Garcia test (c). d Brain water content. *p<0.05 vs sham, @p<0.05 vs vehicle, one-way ANOVA, Tukey’s test, n=6/group.

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