The kallikrein-kinin system is activated in the ischemic mouse brain after stroke as indicated by KNG consumption. Immunoblot from the cortex and basal ganglia of a mouse subjected to tMCAO with the use of an antibody against KNG. The 24 hours after stroke time point is depicted. A sham-operated mouse served as control. Immunoreactivity against native KNG was markedly down-regulated in the brain of the mouse with cerebral ischemia. In contrast, cleaved KNG, which is produced when native KNG is consumed by plasma kallikrein to form bradykinin, was up-regulated in the ipsilateral (i), that is, ischemic cortex and basal ganglia of the mouse with stroke but not in corresponding regions of the brain of the sham-operated mouse or the healthy contralateral (c) hemisphere. Immunoblots were independently replicated from 3 different animals. One representative sample is shown.