Fig. 2.

Ripk2^−/− mice have dramatically lower pro-inflammatory activity and greater BBB preservation in the cerebral cortex 24 h post-stroke compared to Ripk2^+/+ mice. A Heat map of inflammation-associated genes in the ipsilateral cerebral cortex comparing the difference in expression between the two genotypes. Horizontal lines denote individual animals, while vertical lines denote genes of interest. B Quantification of the heat map in (A), depicting mRNA levels of Tnfα, Il1β, Il6, Cxcl1, Ccl2, and Mmp9 in the ipsilateral (CXI) and contralateral (CXC) cortices of the two genotypes 24 h after stroke. C Western blot (WB) of the ipsilateral cortex depicting levels of ZO-1, Occludin, and Active-MMP-9, and β-Actin in Ripk2^+/+ (WT) and Ripk2^−/− (KO) brain homogenate. D–F Quantification of WB shown in C. G ELISA for the detection of the blood serum protein Albumin in the CXI and CXC of WT and KO mice 24 h after stroke, as a measurement of BBB permeability. A, B n = 7/genotype, (C–F) n = 5/genotype, (G) n = 7/genotype. Statistical differences determined by two-way ANOVA, Turkey’s multiple comparison test. *P < 0.05, ***P < 0.001, ****P < 0.0001