Fig. 1.

Deficits of Kir4.1 and MBP expression in both ischemic human patients and tMCAO mice. (a and b) Representative CT brain scans show an epileptic patient before and after the resective surgery (a) and an acute ischemic patient before and after decompressive craniectomy (b). The high density contrast area marked with red dotted line confirms the cerebral infarction of the ischemic stroke patient after decompressive craniectomy. (c) Representative images (left panel) and summary bar graph (right panel) of Kir4.1 and MBP expression levels from 10 non-ischemic surgical patients as comparison and 6 acute ischemic stroke patients, respectively. There is a significant decrease of Kir4.1 and MBP expression in ischemic cerebral tissues compared with that in non-ischemic patients. n = 6 and 10 patients for each group, respectively. ∗∗∗p < 0.001, two-tailed unpaired t-test. (d) The experimental diagram illustrates an established transient middle cerebral artery occlusion (tMCAO) mouse model of ischemic stroke. After MCA occlusion for 40 min, 2,3,5-triphenyltetrazolium chloride (TTC) staining was observed after 24 h reperfusion to detect the extent of the infarction in a series of brain sections. Representative images of Kir4.1 and MBP expression levels of ipsilateral infarction region by Western blottings at day 0, 1, 3, 6, and 9 of the onset of tMCAO. (e) The summary bar graphs show the expression changes of Kir4.1 and MBP in a 9-days time window of tMCAO. Note that both Kir4.1 and MBP show a continuous decrease starting at 24 h after reperfusion of tMCAO, while after the sixth day, they both rebounded synchronously. ∗∗∗p < 0.001. n = 4 mice for each group, one-way analysis of variance (ANOVA) followed by Bonferroni post-hoc tests.