Figure 5.
Figure 5. PPK deficiency reduced tPA-induced BBB leakage after ischemic stroke. (A) Representative images of Evans blue extravasations from WT and Klkb1−/− treated with saline or tPA (10 mg/kg) and euthanized at 24 hours after stroke. (B) Quantification of Evans blue fluorescent intensity for each group. Data are presented as mean ± SEM, n = 5-6. *P < .05; **P < .01. (C) Effects of PKal inhibition on tPA-induced neurological dysfunction after ischemic stroke. Neurological severity score was evaluated 24 hours after stroke in WT and Klkb1−/− mice treated with saline or tPA (10 mg/kg). Data are presented as mean ± SEM, n = 5-7. *P < .05. (D) PKal inhibition accelerates reperfusion during tPA treatment after stroke. Quantitative analysis of rCBF showed facilitated reperfusion in Klkb1−/− mice. Laser-Doppler flowmeter was used to monitor rCBF for up to 2 hours and at 24 hours after tPA treatment. Data are presented as mean ± SEM, n = 3-6. *P < .05 vs WT + tPA.

PPK deficiency reduced tPA-induced BBB leakage after ischemic stroke. (A) Representative images of Evans blue extravasations from WT and Klkb1−/− treated with saline or tPA (10 mg/kg) and euthanized at 24 hours after stroke. (B) Quantification of Evans blue fluorescent intensity for each group. Data are presented as mean ± SEM, n = 5-6. *P < .05; **P < .01. (C) Effects of PKal inhibition on tPA-induced neurological dysfunction after ischemic stroke. Neurological severity score was evaluated 24 hours after stroke in WT and Klkb1−/− mice treated with saline or tPA (10 mg/kg). Data are presented as mean ± SEM, n = 5-7. *P < .05. (D) PKal inhibition accelerates reperfusion during tPA treatment after stroke. Quantitative analysis of rCBF showed facilitated reperfusion in Klkb1−/− mice. Laser-Doppler flowmeter was used to monitor rCBF for up to 2 hours and at 24 hours after tPA treatment. Data are presented as mean ± SEM, n = 3-6. *P < .05 vs WT + tPA.

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