Skip to main content
Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

Global deletion of Ripk2 dramatically reduces infarct volume after transient ischemic stroke. A Western blot (WB) of RIPK2 in the cerebral cortex homogenate from Ripk2+/+ (WT) and Ripk2−/− (KO) mice under naïve conditions. B Representative TTC staining of 1 mm-thick coronal brain slices from Ripk2+/+ and Ripk2−/− mice 24 h post-tMCAO. C Quantitative analysis of total infarction in each brain region. D Quantification of the infarction measured from each individual 1-mm-thick slice at the levels of the subcortex, cortex, and total hemisphere. A n = 5–6/group. B–D Ripk2+/+: n = 14, Ripk2−/−: n = 13. Statistical differences determined by Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

Back to article page