Fig. 6: Ischemic stroke facilitates ZT-1a entrance into the brain.
From: Modulation of brain cation-Cl− cotransport via the SPAK kinase inhibitor ZT-1a
a Anti-serum-albumin-labeled brain sections at 24 h after sham or tMCAO surgery illustrate image collection in the perilesion and contralateral (CL) control areas (white boxes). Note that tMCAO-subjected mice exhibited increased serum-albumin immunofluorescence intensity in the ipsilateral (IL) hemisphere compared with that of sham mice. b Higher-magnification (×40) images of serum-albumin immunofluorescence. The arrow shows albumin in vessel lumen. The arrowhead shows albumin that has diffused into ischemic brain parenchyma. c Quantitative analysis of albumin immunofluorescence intensity as shown in b. Data are mean ± SEM, n = 5 per group (male); ***p < 0.0001, one-way ANOVA. d Experimental design for bioavailability assay of ZT-1a in mouse plasma and brain. ZT-1a was administered at 3 h post reperfusion or post sham surgery. Blood and brain samples were collected at 2 h post injection. e Plasma ZT-1a concentrations were indistinguishable in sham-operated and tMCAO-subjected male mice (p = 0.29; n = 11 (sham) and 9 (tMCAO)). f Increased ZT-1a concentration was detected in contralateral (CL) and ipsilateral (IL) brain tissues of ischemic versus sham-operated male mice. Data are mean ± SEM, n = 10 (sham) and 11 (tMCAO). **p < 0.01, one-way ANOVA.
