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Fig. 8 | Journal of Neuroinflammation

Fig. 8

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

Fig. 8

Selective deletion of Ripk2 from microglia reduces infarct size and preserves BBB 48 h after stroke. A Schematic paradigm of microglial-specific Ripk2 conditional knockout (μKO) animal generation. B Quantification of Ripk2 expression in WT- and μKO-derived microglia. C TTC staining of WT and μKO brain slices 48 h after tMCAO. D Quantification of total infarct sizes at the subcortical, cortical, and hemisphere levels. E Edema index represented as the ipsilateral hemisphere percentage of the contralateral hemisphere. F–H Quantification of the infarct of each individual 1 mm-thick slice in the subcortex (F), cortex (G), and hemisphere (H). I Representative WB of active and inactive MMP-9 in the ipsilateral cortex of WT and μKO 48 h after stroke. J Quantification of WB in I. K Albumin levels in the cerebral ipsilateral (CXI) and contralateral (CXC) cortices of WT and μKO mice 48 h after stroke. B n = 3/group, Ripk2 mRNA expression normalized to housekeepers 18s and Cyc1. C–H n = 13/group. I, J n = 6/group. K n = 8/group. B, E, J Student’s t test. D–H, K Two-way ANOVA. *P < 0.05, **P < 0.01

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