Skip to main content
Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Receptor-interacting protein kinase 2 (RIPK2) profoundly contributes to post-stroke neuroinflammation and behavioral deficits with microglia as unique perpetrators

Fig. 4

Ripk2−/− mice have smaller infarcts, zero mortality, and better behavioral outcomes 28-day post-stroke compared to Ripk2.+/+ mice. A Experimental design for the 28-day, longitudinal study. B Cresyl violet staining of 30 μm-thick brain slices at 28 days after stroke with inset depicting delineated areas of the infarct. C Quantification of infarct sizes from Cresyl violet-stained sections from each genotype. D Kaplan–Meier survival curve out to 28-day post-stroke. E, F Time required for mice to descend the vertical grid (E) after stroke, quantified in F. G, Distance traveled in the open field chamber (G) after stroke, with each value being normalized to that animal’s baseline distance (H). I, J Weight grip scores determined after stroke. Mice grip weights of increasing mass (I) and scores were quantified (J). K Total neurological deficit score assigned at indicated timepoints after stroke. B, C n = 9–14/genotype. F–K n = 14–21/genotype at 24 h and 48 h, n = 11–14/genotype at 7d, n = 10–14/genotype at 14d and 21d. C Student’s t test. D Gehan–Breslow–Wilcoxon test. F, H Two-way ANOVA. J, K Mann–Whitney test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

Back to article page