PKal inhibition reduces tPA-induced increases in infarct volume and MMP-9 activation after stroke. (A) Representative coronal sections of 2,3,5-triphenyltetrazolium chloride–stained brain sections of mice at 24 hours after ischemic stroke. At 2 hours after stroke onset, mice received tPA (10 mg/kg) either alone of following a 15 minutes pretreatment with BPCCB (1, 3, 10 mg/kg) or saline vehicle. Klkb1^−/− mice were treated intravenously with saline or tPA (10 mg/kg). Ischemic infarctions (white color area) were detected in all groups; however, tPA alone showed a remarkably ischemic volume. (B) Quantitative analysis of infarct volume at 24 hours after ischemic stroke. *P < .05; **P < .01; ***P < .001. Data are presented as mean ± SEM, n = 5-8. Numbers in x-axis labels for panel B indicate concentrations of BPCCB in mg/kg. (C) Coadministration of PKal inhibitor BPCCB with tPA decreases MMP-9 activation in brain after stroke. Representative zymographic analysis of brain extracts from sham and stroke mice treated with vehicle, tPA (10 mg/kg), or BPCCB (10 mg/kg) after MCAO and analyzed at 24 hours after stroke. (D) Quantitative determination of zymographic gels for each treatment. Data are presented as mean ± SEM, n = 5. *P < .05; **P < .01.